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Immunology Online Question Compilation -2004

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Beggar’s can’t be choosers. The best answer, that scored all points and used the concept “Brevity is key,”
from each question, was selected for compilation. In few instances, answers were slightly altered, or
combined with another answer and/or Waterborg’s suggestions, to make the answer more complete.
Questions not answered are listed at the end. The information within these notes may change without
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Lecture 1 – Immunology Online Questions; Chapter 1
1. Pathogens are caught by specialized immune organs with a surveillance function. Describe the
filtration mechanism of one such organ. From where do microbes originate that are trapped by this
The spleen specializes in filtering blood-borne pathogens. Its tissues are composed of white pulp and red
pulp. The white pulp contains lymphocytes and lymphoid follicles, while the red pulp is composed of a
network of open vascular channels (sinusoids) bathed in the blood flowing through the organ. Phagocytes
and dendritic cells lining the sinusoids assist in immune responses by trapping blood-borne pathogens.
Phagocytes will ingest and destroy these microbes, and the dendritic cells will gather antigens/pathogens
and present them to the lymphocytes in the white pulp. The microbes going through the spleen are located
in the blood and either penetrated an epithelial barrier, entered the lymph system from subcutaneous
tissue, and were consequently dumped into blood circulation; or were brought there by an infected cell
moving between the lymph and blood vessels.
The lymph nodes have a filtration mechanism along the lymphatic channels throughout the body. Fluid
that is drained into the lymph nodes comes from lymphatics which carry fluid from epithelia and
connective tissue. Antigen Presenting Cells (APC) monitor the antigens of microbes that may enter
through connective tissue to the lymphatics. Another filtration mechanism of the lymph node is to have
dendritic cells grab antigens of microbes from epithelia and take antigens back to the lymph node. The
microbes found in lymph nodes are lymph-bourne antigens, and they enter through epithelia or other
colonizing tissues.
2. Describe how circulating T lymphocytes can exit from the blood circulation and enter a lymph
node. How do these T cells exit the lymph node?
The thick endothelial cells on the inside of the venule (HEV) bind to t cells and they [the T cells] travel
[in]to the lymph nodes. Chemokines secrete chemotactic signals causing cells to go to the right location. T
lymphocytes recirculate by coming out of arterioles and are picked up by efferent lymphatics which
drains into the thoracic duct. This is important because it distributes antigen detection throughout the
body, other lymph nodes, spleen, tissues and organs.

Chapter 1 1. and must physically contact microbes to destroy them. Why can they not fight most bacterial infections by remaining in the blood circulation? Although neutrophils and monocytes do ingest microbes in circulation. 2. Examples of Phagocytes are Circulating Phagocytes. contained on Phagocytes. Polysaccharides are common in the mammalian body. they would only be effective against microbes that entered the bloodstream. making them hard to be recognized as foreign structures. This is because sites of infection are often extravascular. and thus they cannot escape the innate detection by the LPS-receptor bearing phagocytes. . and phagocytosis requires direct contact with the microbe. This is illustrated by leukocyte adhesion deficiencies. Gram-negative bacteria cannot exist without LPS. making it an easily identified as foreign. but LPS is essential for the function of porins as part of the transport system for hydrophilic molecules. While a B-cell can send antibodies to fight infections. Tissue Phagocytes are of Macrophages lineage and include Microglia. A change in these LPS would be a trade off of enhanced phagocytic protection for a loss in epithelial survival ability. became involved). Lecture 2 – Immunology Online Questions.coli cannot prevent detection by the macrophage LPS receptor and thus prevent phagocytosis. One example is the receptor. The components of innate immunity recognize structures that are shared by various classes of microbes and are not present on host cells. Explain why Gram negative bacteria like E. All gram negative bacteria have LPS in their cell walls. folding or location. some LPS resist the action of peptide antibiotics. where leukocytes are unable to effectively exit blood vessels. which kills the microbe by release of enzymes. The result is increased susceptibility to infections. by the Pattern Recognition Receptors located on Phagocytes. LPS is a combination of lipoproteins and polysaccharides that are found nowhere in mammalian organisms. Detection of LPS is further enhanced because all macrophages have the TLR-4 receptor for LPS. it is because of the polysaccharide layer of the outer capsule. including Neutrophils and Monocytes.3. Binding of the microbial characteristic to the receptor activate the Phagocyte. The phagosome then fuses with the Lysosome forming a Phagolysosome. The bacterium could try to hide LPS from macrophages by changing its sequence. extravascular bacteria would be given relatively free reign to multiply and infect at will (until other immune system defenses. Meanwhile.brIf these cells were to remain in circulation and attempt to fight an infection. 4. Also. Often when a bacterium evades phagocytosis. Changes in LPS would inhibit normal membrane transport. but not on mammalian cells. How is this feature recognized? Name one cell with innate detection and response capabilities. for bacterial Lipopolysaccharide (LPS). such as Phagocyte Oxidase and other toxic substances produced in the Phagolysosome. a phagocytic cell has no similar ability. This feature is recognized as a Molecular Pattern. Kupffer Cells and Osteoclasts. Binding promotes ingestion of the microbe into the Phagosome. promoting phagocytosis and killing of the microbe. they typically must exit circulation to attempt phagocytic eradication of infection. What is the chemical composition of the macrophage-produced innate cytokines TNF and IL-1? Are these two cytokines also chemoattractant chemokines for neutrophils? Explain your answer. This is present on Gram-negative Bacteria. Explain why neutrophils and macrophages typically must exit the blood circulation in order to attempt phagocytic eradication of a bacterial infection. such as adaptive immunity. Name one characteristic of bacteria that is used by cells of innate immune responses to detect them.

Therefore TNF and IL-1 are not chemokines but they do directly induce the production of them from endothelial cells. Lecture 3 – Immunology Online Questions. Microbe is phagocytized and fused w/ a lysosome forming a phagolysosome. 3. ROI are three distinct microbial mechanisms by which activated macrophages kill endocytosed bacteria. the endothelial cell will express selectin adhesion molecule for the binding of leukocytes. above except lysosomal proteases are the enzymes that kill the phagocytized microbes but dont harm the phagocyte. When TNF and IL-1 encounter endothelial cells they respond in two ways. along with the chemokines produced by macrophages. However. Secondly. Same phagocytic scenerio as in 1. It notifies the macrophage or neutrophil to eat me. that cause the chemotaxis of leukocytes to the endothelium. 3. the endothelial cells will express its own cytokines called chemokines. Summary: iNOS. List at least 3 distinct microbicidal mechanisms by which activated macrophages kill endocytosed bacteria. C3b starts the late steps of complement activation and makes a collection of the peptides and polymerized C9. Same phagocytic scenerio as in 1. These two cytokines are not chemoattractant chemokines. NO. during a strong response.TNF and IL-1 are soluble proteins that mediate immune and inflammatory reactions and are responsible for communications between leukocytes and between leukocytes and other cells. Receptors on the surface send a signal to activate the enzymes in the phagolysosomes. 1. the lysosome can dump its contents prematurely injuring tissue surrounding the phagocyte. First. but they do influence the production of the compounds. 4. Phagocyte oxidase kills microbes by converting molecular oxygen into superoxide anion and free radicals or ROIs and are toxic to the microbe. inducible nitric oxide synthase catalyzes the conversion of arginine to nitric oxide. We say that C3b is an "opsonin". It is these chemokines. What does this mean? What process is accelerated by C3b opsonization of bacteria? Opsonin is a macromolecule that enhances phagocytosis by attaching to the surface of a microbe that is recognized by a surface receptor of a neutrophil or macrophage. 2. The C3b accelerates the complement system by binding to the microbe to activate proteins further down stream. Chapter 2 . above except another enzyme.

Match up all pairs of molecular interactions among the following protein surfaces when a T cell interacts with an APC: 1. B and C ? . 3. 4. Some other polymorphic residues allow variations in the top of hte clefts which helps with its recognition by T cells. amino acid side chains of a presented antigenic peptide. Therefore bacteria X must be phagocytosed and digested into peptide fragments that can then be combined with newly formed MHC molecules. (2:5)The Polymorphic alpha-1 and beta-1 chains of MHC-II molecules also interact with the AA Side Chains of a presented Antigenic Peptide. MHC molecules are configured to present peptide fragments (usually). If these few amino acids are able to fit into the site. Why do nucleated cells in most humans express 6 different forms of MHC-I molecules if the human genome at the HLA locus only contains 3 genes. Yet MHC molecules are only loaded with antigens during their formation in the ER. they they will be able to bind and be held in the cleft. 2. polymorphic MHC side chains on the alpha-helices of the alpha-1/alpha-2 MHC-I protein module. 2. (1:4) The polymorphic MHC side chains on the alpha-helices of the alpha-1/alpha-2 MHC-I protein module interacts with the Ag-specific detection surface of the T cell receptor. polymorphic amino acid side chains on the anti-parallel beta-sheets of the MHC protein. This occurs when an ER vesicle carrying the MHC molecule fuses with an endosome containing the peptide fragments. However. the antigen-specific detection surface of the T cell receptor. 3. Also the side chains of the various amino acids in the peptide antigens fit into MHC pockets and keep the side chains in the cleft.1. Explain how the structure of the MHC presentation cleft can bind and hold many different peptides that may have only peptide length and 2 or 3 amino acids in common. CD4+ T cells only recognize extracellular antigens when they are presented on MHC II molecules on other cells surfaces. forming anchor residues that may bow upward to interact with the Antigen Receptor of T Cells. (2:3)The AA side chains of the Presented Antigenic Peptide also react with the beta-sheets in the floor of the MHC molecule may bind the AA side chains on the Presented Antigenic Peptide. 4. Explain why a clone of T cells that is specific for extracellular bacterium X only detects proteinderived antigenic fragments following phagocytosis and disassembly of bacteria X by a macrophage APC. The polymorphic residues contribute to the different ways the floor of the peptide binding cleft and in turn allow the MHC molecules to bind different peptides. As long as the MHC molecule is able to change allosterically to accomodate these residues from the peptide theyll fit into an MHC molecules cleft. forming a cleft that can accommodate peptides of 10-30 AA. 5. the non-polymorphic beta-2 domain that binds CD4 can only respond to peptides presented by MHC-II molecules. The loaded MHC molecule is then carried to the cell surface where it can be recognized by the T cell. (1:2)The Amino-terminal alpha-1 and alpha-2 domains of the class I MHC molecule interact with the AA Side Chains of a presented Antigenic Peptide to form a peptide-binding cleft that can accommodate the peptides of 8-11 Amino Acids (AA). non-polymorphic amino acid side chains on the anti-parallel beta-sheets of the MHC protein. (2:4)AA side chains in the peptide antigens fit into the pockets in the floors of the peptide binding clefts of most MHC molecules. named A. The MHC presentation cleft is an allosteric site and is able to change according to what peptides are bound.

CD4+ helper T cells can only respond to extracellular antigen because extracellular microbes are captured by APCs and are presented by class II molecules. Describe clearly why MHC-I presentation proteins can only be loaded by peptides derived from cytoplasmic proteins and can NOT be loaded which peptides generated from extracellular antigen. it is able to resist proteolysis by endosomal proteases. the immune system is able to respond to intra and extracellular microbes in the best way possible. Unlike secreted IgM. Since you get 2 sets of 3 alleles. and transported into the ER by TAP. In addition. being stable. when cytosolic peptides enter the ER they can be captured by class I. By segregated the class I and class II pathways of antigen processing. MHC I presentation proteins can only be loaded by peptides derived from cytoplasmic proteins for a couple of reasons. 6 different forms of MHC-1 molecules can be expressed.associated peptides are recognized by CD4+ T lymphocytes which function as helper cells). 3. The immunoglobulin is a heterodimer with two light and two heavy chains. but now the class I molecule is not available to bind peptides. In addition. membrane IgM does not have a valence of 10 due to splicing of the c-terminal.the fragment for antigen binding. Crosslinking of two or more Ig receptors causes the tyrosin kinases to phosphorylate themselves and signal transducation to result. thus activating the 2 effector mechanism that eliminates extracellular and ingested microbes. CD4 has specificity for Class II (class II. These chains are joined by covalent inter and intramolecular disulfide bonds for stabilization of each globulin domain. CD4 has specificity for class II MHC molecules. but not class II b/c they are tied up w/ the invarient chain. The helper T cells help B lymphocytes to produce antobodies and phagocytes to ingest and destroy the microbe. The BCR is consists of IgM or IgD flanked by two helper proteins.Nucleated cells in most humans express 6 different forms of MHC-1 molecules if the genome at the HLA locus contains 3 genes: A. and C. a protein not found in the cytoplasm will not be tagged by ubiquitin for proteolysis and will not be available for TAP to transport into the ER. What are "CDRs"? How many CDRs create the B cell receptor surface that recognizes presented antigen? . A and B. These are the sticky parts of IgM. Once the complex is formed. the peptides that bind to MHC I molecules have to be ubiquinated in the cytoplasm. 2. Therefore. The BCR has two paratropes. degraded by a proteosome. it is stabilized and transported to the cell surface. B. Lecture 4 – Immunology Online Questions. The shape of Ig is composed of anti-beta sheet domains linked together. First. 4. Cytosolic antigens are presented by class I MHC molecules that are processed by CD8+ T lymphocytes (not CD4+). This is due to the fact that all alleles are expressed on MHC molecules / genes from both the maternal and paternal side (codominance). Explain the basis why CD4+ helper T cells can only respond to extracellular antigen. As the peptides enter the ER they are captured by an MHC I molecule. The Ig itself only binds an antigen. the class I-peptide complex may intersect endosomes. Describe the structural features of the B cell immunoglobulin receptor protein that determine protein shape and prevent the separation of Ig polypeptide chains. Chapter 3 1. This codominant expression allows increased Ag-peptide presentation. The Cterminus is hydrophobic so it will stay in the membrane. during transport. The signal is transmitted throug the associated A and B chains. and. The chains have a variable N-terminis created by somatic recombination.

Because the Fc region on a membrane bound IgG is contained within the B cell. which activate B-cells to secrete Antibodies and activate macrophages cannot happen. the above process cannot occur. a single antigen can activate mulitple B-cells because many B-cells in the body can recognize the same or distinct epitope on that antigen. This is the total strength of binding of the interaction and is much greater than the affinity of a single antigen-antibody bond. Explain how effector cells like macrophages can use secreted IgG to detect. These antibodies coat microbes and promote their ingestion. while IgG binds the weakest. they were secreted by B cells that arose by various developmental pathways from a single naïve B cell progenitor cell). 2. In the human body. called FcyRI (CD64) which bind to certain antibody isotypes IgG1 and G3 in humans. A bacterium is exposed to a mixture of secreted IgM. How many different epitopes could be recognized by antibodies in "A"? Explain your answer. . bind and digest adaptively opsonized bacteria. Any B-cell that can recognize the epitope within the human serum can secrete Ig to be included in the antiserum. Its function to alert Cd4 and helper t_s. 1. They all recognize an abundant carbohydrate surface antigenic epitope. This process and their subsequent phagocytosis is called opsonization. List all factors that contribute to creating the full paratope reservoir of T lymphocytes. with ten antigen-binding sites. All paratopes on the surface are the same becuase a B-cell only makes a sinlge BcR from a single Ig gene and can only detect one specific eptitope. Which antibody binds strongest and which one weakest? Explain your answer. Chapter 3 1. making a total of 6 CDRs per B cell receptor surface. the stronger the multiplied cross-reaction. Effector cells like macrophages express a high affinity receptor for the Fc regions of gamma chains.e. Explain why the B cell receptor of the activated B cell (which secreted the IgG antibodies) cannot serve this role.How many different B cell clones secrete Ig in "B"? 2. A combination of 3 CDR(H) and 3 CDR(L) loops creates an Ag binding site. Chapter 4 1. but due to the avidity of the interaction. both raised using the same antigen: 1. an array of Fc regions is formed projecting away from the microbe which bind to the macrophage high affinity regions. When taken from body all of the antibodies from B-cell clones that recognized the Ag epitope are inlcuded in the antiserum. IgG and IgA antibodies that all have identical paratopes (i. The antibody IgM.CDRs are complementary determining regions that form loops in the N-terminal Ig domain of the H and L chain. Lecture 6 – Immunology Online Questions. 2. IgA has four antigen-binding sties. binds strongest to the abudant carbohydrate surface antigenic epitope. When several antibody molecules bind to a microbe. This total strength occurs through multiple Ag-Ig interactions. so the more antigen-binding sites the Ig has for the epitopes of this antigenic carbodydrate surface. Lecture 5 – Immunology Online Questions. Only one epitope can be recognized by a monoclonal antibody producing B-cell because only a single clone is isolated and cultured that recogneized the particular Ag epitope. There are 3 CDRs per Ig domain. 3. The strengths are not only due to the number of antigen-biding sties each Ig has. having two antigenbinding sites. They are also known as the hypervariable parts of each V domain. When one compares a monoclonal antibody preparation (A) with a polyclonal antiserum (B).

When lymphocytes develop in generative lymphoid tissues and start to recombine their Ig or TcR genes in order to attempt to create a functional antigen-specific receptor. cells die. and number of genomes. The name of this process is negative selection. number of joining gene segments. there is only one type of paratope that can be created. the cells would not pass through the checkpoints of maturation. IL-2 can also be called the T-cell growth factor. In each such case. As a result each B cell produces either one kappa or lambda light chain from one of the parental alleles. After this allelic exclusion it goes through a second exclusion with the Ig light chains first kappa and then lambda. When IL-2 binds to the IL-2 receptor the binding will stimulate the T cells to enter the cell cycle and to begin to proliferate and then there is an increase in the number of the antigen-specific T cells. Describe one situation that leads to cell death. 3. All other alleles are excluded from being active and end up going through apoptosis by neglect. then it will be doomed to start apoptosis. and ligation of the ends. After these chance events. Interleukin 2 (IL-2) is considered an essential cytokine for any antigen-specific lymphocyte response. Chapter 4 1. Junctional diversity includes removal of nucleotides by exonuclease. is this an active or passive process? What is the name of this type of lymphocyte selection? One situation that leads to cell death would be when a gene is produced that does not code for amino acids after gene recombination. Combinational diversity includes number of V gene segments. The process by which the cell start apoptosis is passive because the cell dies as a result of not receiving survival signals and not from any action on the cell. Why do we call the T cell proteins CD4 and CD8 "co-receptors"? What is their contribution to . If the recombination can't produce one good chain used for the antigen receptor. 2 in the first process and 4 in the second it exits the bone marrow to become mature. There are two processes that are activated by the mu protein and the pre-BCR complex signal. These processes of allelic exclusion ensures that each cell can express receptors of a single specificity. 4. Since it has this specificity. The TcR would still be used as the receptor on a pro T cell. many attempts fail. Which process is driven by the IL-2 receptor signal? IL-2 acts to stimulate the proliferation of T cells. addition of uncoded nucleotides. a nonsense codon is produced which cause the translation of the protein to stop there and the rest of the receptor would not be completed. However. naïve B cells when they exit the bone marrow. Lecture 7 – Immunology Online Questions. For the example you describe. One of the processes actually shuts the recombination of the Ig heavy chain genes on the second chromosome because each B cell can express IG from only one of the two inherited parental alleles. number of diversity gene segments. Explain how the developmental B cell process named "allelic exclusion" will have created only ONE paratope on the surface of mature.The factors that contribute to creating the full paratope reservoir of T lymphocytes can be divided into two main categories: combinational diversity and junctional diversity. Thus. 2. Instead.

The IL-2 receptor exists on Naive T-cells as a two chain molecule. which when combined with the first two. There are two subsets of helper T cells : Th1 and Th2. Which important cytokine induces differentiation of helper T cells to support an immune response with phagocytes as primary effector cells? Which leukocyte secretes this cytokine? IL-12 is a cytokine that induces the differentiation of helper T cells. whose differentiation is promoted by IL-12. thus the majority of the cytokine exists around the T-cell). IL-2 has been identified as a cytokine that is required for lymphocyte proliferation. Two or more TCRs and coreceptors need to be engaged to initiate a response. integrin. Macrophages and dendritic cells produce the IL-12 in response to bacteria and viruses. 4. B7 is a ligand 5. produce IFN-gamma which stimulates the phagocyte-mediated killing of ingested microbes. Explain why production of the alpha-subunit of the IL-2 Receptor results in effective IL-2 stimulation of T cell proliferation at reduced concentrations of IL-2. Describe the mechanism by which IL-4 enhances the non-phagocytic immune response and . results in proliferation. CD4 is a receptor 4. CD3 is a receptor 7. These proteins contribute to creating a TCR signal by recognizing different classes of MHC molecules. MHC-II is a ligand 8. CD28. The clustering of CD4 or CD8 coreceptors activates a tyrosine kinase called Lck that is attached to the cytoplasmic tails of the coreceptors. 2. ICAM-1 is a ligand 6. MHC-II. ICAM-1. B7. it will express the third chain of the receptor. When the T-cell becomes activated. even at reduced concentrations of IL-2. (kd of 10^-11 as compared to 10^-9 for the two chain molecule). Chapter 5 1. CD4. Identify for each of the following leukocyte cell surface proteins whether it is a Receptor (or part of a Receptor) [R] or whether it is a Ligand [L]: alpha-beta TcR heterodimer. 1. The CD4 and CD8 proteins are called coreceptors because they function with the TCR to bind MHC molecules.creating a TcR signal? The T cell receptor for antigen (the TCR) and the CD4 or CD8 coreceptor work together to recognize the complex of peptide antigens and MHC molecules. CD3. Alpha-beta TcR heterodimer is a receptor 2. (the T-cells secreted IL-2 works on itself. Th1 cells. Lecture 8 – Immunology Online Questions. integrin is a receptor 3. This high affinity combined with the autocrine effect. has a very high affinity for IL-2. CD28 is a receptor 3.

Specifically. Chapters 5 & 6 1. It allows them to stay long enough to eliminate the microbe. which binds to the Fc end of the Ab via the receptor. producing products that bind to the phagocyte complement receptors. 2. They attach to the endothelial cell by integrin interactions and migrate to the site of infection by moving toward the concentration gradient of chemokines. if you were to have only macrophages and the CD4+ DTH response the intracellular bacteria would not be killed. which normally produce the cytokines necessary to generate a nonphagocytic immune reponse. The other T cells do not bind there and they return to circulation. Together these two systems work together by injesting the bacteria in the macrophage (which will escape into the cytoplasm) this will signal the . Intracellular microbial infection of tissue macrophages causes antigen-specific CD4+ effector T cells to be concentrated in the infected tissue. TH cells do not differentiate into the TH2 subset. l-4 is produced by TH2 cells. APC_sexpress more MHC II molecules and the B7 costimulator inorder to engage more T cells and produce a good response. that are not specific for the microbe. Why do antigen-specific T cells respond in this manner? Why are other CD4+ T cells. 3. The cytokines produced by macrophages also cause the endothelial cells to express more selectins and integrin ligands(ICAM-1 and VCAM-1). and the CD4+ DTH responce is unable to provide anything else that could. The macrophage is unable to kill itself or the bacteria.selectin ligands and the integrins LFA-1 and VLA-4. This combination is important against parasitic worms and helminths. not found at high concentrations in the infected tissue? The antigen-specific T cells become concentrated in the infected tissue because the expression of their adhesion molecules increases as they become activated.suppresses the phagocytic immune response. Any effector T cells can enter. therefore the bacteria is able to live and infect the host. Using Listeria as an example. and can create a positive feedback loop that makes more TH2 cells by activating effector CD4+ T cells to differentiate into TH2 cells. These bacteria types have the characteristic of being able to escape the vessicles within phagosome and live in their cytoplasm. Describe the mechanism by which IFN-gamma enhances the phagocytic immune response and suppresses the non-phagocytic immune response. Lecture 9 – Immunology Online Questions. the antigen-specific T cells are again stimulated by the microbe and they adhere firmly to tissue by an increase in expression and binding affinity of VLA integrins. This part is not antigen-specific. therefore. As a result of IFN-G production. Describe the important characteristic(s) of a species of intracellular bacteria that infects macrophages and that cannot be eradicated by a CD4+ DTH response alone nor by a CD8+ CTL response alone. if acting alone is not able to elimate the bacteria if it is not in the cytoplasm of a cell. It also stimulates the B cells to produce antibodies (IgG1 and IgG3good opsinizing Ab) that will opsinize the antigen for recognition by the phagocyte. In the case CD8+ CTL responce. Ab also activates the complement system. however. the adhesion molecules that are expressed are the high affinity forms of P. IFN-G supressess the non-phagocytic response by inhibiting the IL-4 cytokine pathway. IFN-F production from a TH1 subset cell enhances the phagocytic immune response by activating macrophages to kill the microbes. IL-4 stimulates IgE production and IL-5 activates Eosinophils.and E. It also inhibits activation of IFN-gamma production which would stimulate macrophage activation.

This is how complement-opsonization of bacteria can enhance B cell immune responses. Chapters 6 & 7 1. Explain the role each factor plays in B cell activation. is recognized by the CR2 receptor on B lymphocytes. Signals delivered by this receptor stimulate B cell responses against the microbe. Natural killer cells are activated in this situation b/c of the deminishing surface expression of class I molecules. Lastly. One way a virus can evade the CD8+CTL cell is by ihibiting or reducing the amount of MHC1 molecules. Explain how complement-opsonization of bacteria can enhance B cell immune responses. ii) Increase in expression of cytokine receptors. In T dependent responses there is isotope switching shown. Nonprotein Ag are called T-independent Ag because they elicit the Ab response without the involvement of the T cell. or cytokine receptors. List at least two processes. to be actived. that recognizes the Ag presented by the B-cell. or by removing newly synthesized class 1 molecules from the ER. Complement proteins bound to antigene-antibody complexes are recognized by follicular dendritic cells in germinal centers. iii) Reduction in receptor expression on these cells for chemokines. memory B cells production. The complement system provides stimuli for the development of humoral immune responses. early during the process of antigen stimulation. upon what happens in (ii) and (iii). All these viral mechanisms reduce the loading of class I MHC molecules by viral peptides. . activated B-cells migrate out of the follicle to the periphery where they will encouter the helper T-cells. but in T independent responses this secondary response is only seen in response to some Ag. Describe TWO mechanisms by which a virus can evade an effective CD8+ CTL cell-mediated immune response. Antigen-mediated B-cell activation causes: i) Increase in B7 expression on these cells. However. to pick up cytokines like IFN-gamma in order to reduce the amount of cytokines that can trigger the cell-mediated immune response. 3. The second way is to produce inhibitory cytokines. 2. 2. Clearly state for each mechanism whether it will invoke NK activation or not. When C3 is activated by a microbe. This can be done by inhibiting expression of class 1 molecules. that are produced in follicle and function is to keep the B-cell in the follicle. in T dependent responses there is a secondary response. This complement-dependent antigene display is another way in which the complement system promotes antibody production. Also less affinity maturation is shown in T independent responses. one of its breakdown products. List functional features of a T-dependent humoral immune response that generally do not exist or occur during a T-independent (so-called TI) response. compared to the T dependent response. receptors or changes in gene expression in B cells. Explain how a B cell can change its effector function by changing its H-chain isotype without changing its paratope. Lecture 10 – Immunology Online Questions.CD8+CTL responce to come and kill the infected macrophage thus killing off the bacteria. Ab response to T independent Ag show less heavy chain class switching (but there may be some IgG). which are secreted mediators of helper T-cell function. allowing the antigens to be displayed for further B cell activation and selection of highaffinity B cells. C3d. 3. which functions as a costimulator to provide a second signal that is required for the T-cell. that prepare B cells for effective interaction with CD4+ helper T cells. This way will not activate NK cells.

Which molecular process. the Poly-Ig receptor. The components of the alternative pathway c-3 convertase are : c3 (the component) and factor B. applied to V-exon DNA sequences of productive H. The components of the Classical Pathway C-5 convertase are C4b. from helper T cells. the only thing that was switched was the handle and the specificity was maintained due to the VDJ being preserved. Monomeric IgA cannot be secreted due to the fact that for it to be transported and cleaved it must be polymeric. The Poly Ig receptor is needed because once it transports through the epithelium part of remains attached to the IgA and part will still be in the membrane following cleavage. The molecular process that is required for affinity maturation to occur is somatic hypermutation. Describe how this factor prevents or limits complement activation. A membrane protein that inhibits complement activation is DAF or Decay Accelerating Factor. . This signal may induce Ag dependent recombination of switch regions such that the VDJ gene is moved closer to a C gene. The follicular dendritic cells display the antigen and only B cells that recognize the antigen are selected to survive. Give the name of one soluble plasma serum protein or of one cell surface membrane protein that inhibits complement activation or destroys active complement complexes. 4. As more antibody is produced the amount of available antigen decreases so the B cells that are selected must have higher affinities to bind to the antigen. It is carried out by a special Fc receptor. These mutations result in the generation of different B cell clones whose Ig bodies have varying affinities to the antigen that initiated the response. is required so that affinity maturation can occur in populations of activated B cells? Explain why. this disruption will terminate complement activation by both the alternative and classical pathways. 4. DAF disrupts the binding of Factor B to C3b or binding of C4b2a to C3b. So. This switch recombination brings the VDJ adjacent to a downstream C region. The active protease is Bb. Without this there would be nothing to cleave and it would not be transported or released.In order for a B cell to undergo heavy chain class switching. determined by the C region.and L-gene loci in B cells. List the names of the components of an Alternative Pathway C3-convertase and of a Classical Pathway C5-convertase. The receptor will then be cleaved by a protease. only B cells with the higher affinity of paratope for epitope survive. Lecture 11 – Immunology Online Questions. endocytose it into vesicles and transport is across to the luminal surface. over time. Describe the process by which polymeric IgA is secreted into oral and gastro-intestinal mucosa. 2a and C3b. This receptor will bind the IgA. Chapters 7 & 8 2. it must receive a signal. Clearly name in each complex the active protease. The result is that the B cell begins to create a new heavy chain.The IgA will then be released with a portion of the bound receptor. yet maintains its specificity as the original B cell because the specificity is determined by the VDJ. This is a Ig mutation which has a frequency of occurring one in 1000 base pairs which is much higher than that of regular genes. 3. Thus the strongest affinity B cell will bind to the antigen leaving the lower and unchanged affinities to die of neglect apoptosis. such as CD40 or cytokines. The active protease is C2a. Why is monomeric IgA not secreted? Polymeric IgA is transported through the epithelium.

These include histamine. mast cells degranulate and release mediators and cytokines. First. and smooth muscle contraction. 1. Chapters 9 & 11 1. which process is more important: "negative selection" or "positive selection"? Explain your answer. however. Immediate hypersensitivity is caused by an excessive immune response to one or a few antigens. the production of cytokines such as TNF and IL-4 lead to the late phase reaction and recruitment of neutrophils and eosinophils. Which cell(s) or molecule(s) cause tissue destruction? Antigens which produce immediate hypersensetivity are often called allergens. Also hypersensitivity diseases can be identified and classified by their mechanism of tissue injury. 2. TH2 cells also play a role by producing IL-5. Which immune effector is produced in excessive amounts? 3. resulting in tissue injury. which are in particular important agents of tissue injury. Lecture 14 – Immunology Online Questions. one could ultimately result in a potentially lethal autoimmune disease from the lymphocytes attacking self antigens present all through out the body.Lecture 12 – Immunology Online Questions. increased vascular permeability. or it may be caused by an immune response that is directed against self antigens which is a result of the failure of self tolerance. Further. which will result in damage to the host tissue as well. Chapters 8 & 9 1. Both play a critical role in the development of central tolerance in T lymphocytes. If this process were not controlled by elimination through negative selection. When one describes the development of central tolerance in T lymphocytes. It is a reflection of excessive or aberrant immune responses. Prostaglandins and leukotrienes also contribute to the vascular dilatation and smooth muscle contraction. Positive selection. What feature or result is required to identify an immune response as a "hypersensitive disease"? Hypersensitivity is an immune response to an antigen that may result in a sensitivity to challenge with that antigen. and this function does not seem to be nearly as important as getting the potentially lethal T lymphocytes who interact with the self antigens in a manner in which they should not. Negative selection is the process by which developing lymphocytes that express antigen receptors specific for self antigens are eliminated. Define the general term "hypersensitivity". Tissue destruction is caused by several agents. Lecture 13 – Immunology Online Questions. IgE is the immune mediator which is produced in excessive amounts. The two conditions mentioned above are the common features in identifying a hypersensitivity disease. but negative selection is more important. ensures that mature T cells are self MHC restricted and that CD8 T cells are specific for complexes of peptides with class 1 MHC molecules and CD4 T cells for complexes of peptides with class II MHC molecules. which activates eosinophils. Chapter 11 2. What is an alternate name for this type of antigen? 2. Protease release can also lead to significant damage of surrounding tissue. Describe two mechanisms by which a tumor which initially was detected by the immune system . which produces vascular dilatation. This may be caused by responses to foreign antigens that may be dysregulated or uncontrolled.

Chapter 10 1. resulting in growth and metastases. What is the reaction that causes the disease state in the example you have described? 2 answers submitted. Questions not viewable because there were not 6 answers submitted: Lecture 14 – Immunology Online Questions. the class(es) of presenting MHC molecules and the type(s) of T cells involved in the anti-tumor response following necrosis. For instance. Describe one example of an auto-immune. is the antigen soluble or is it a tissue antigen? In your example. Identify the antigen in your example and the result when the IgG binds to the antigen. 4. however. Chapter 11 3. Lecture 15 – Immunology Online Questions. Lecture 12 – Immunology Online Questions. Chapter 10 No answers submitted at time of compilation. some tumor cells stop expressing the antigens that are the target of the immmune attack. . rendering them unable to display antigen to CD8+ T cells. Describe a hypersensitivity disease that involves activation of complement. Tumors which have been identified by the immune system and are being prevented from growth and proliferation have several recourses which will permit them to overcome inhibition by the immune system. some tumors stop producing the antigens which the immune system targets. 3. In order for the immune response to be effective it must kill all the tumor cells which not only have the ability to grow rapidly but have certain mechanisms that help the tumor evade the immune system. immune tolerance and immune deficiency in terms of antigen involvement and the immune response that is observed. Identify clearly the cell(s) which present tumor antigens. Second. Other tumor cells can stop expressing class I MHC molecules and thus cannot display the tumor antigen to CD8 T cells. the tumor can go undetected while growing rapidly and metastizing. these tumors are referred to as antigen loss variants. Lecture 13 – Immunology Online Questions. IgG-mediated hypersensitivity.and prevented from growth and proliferation. Explain why experimental vaccination with tumor genes is likely more effective as an anti-tumor immune strategy than vaccination with tumor-specific antigenic proteins. some tumors can also produce immuno-suppressive protiens or cytokines. 0 answers submitted. First. In your example. On a related note. can evade immune detection. 1 answers submitted. that this process leaves the tumor vulnerable to natural killer cells which target cells lacking class I MHC molecules. some tumors cease to express class I MHC molecules. hence. such as transforming growth factor beta. What are the differences between immune reactivity. These tumors are called antigen loss variants. Explain how a tumor that causes tissue necrosis with associated tissue inflammation is more likely to become a target of anti-tumor CTL action than a tumor which does not cause tissue necrosis. is this an auto-immune response? What antibody isotype(s) can cause this disease? 1 answers submitted. It is worth noting. The immune response to tumor cell growth is an on going challenge. Chapters 9 & 11 1. Therefore.

4. second-signal provided to the antigen-specific helper T cell. created by apoptosis. Explain how a microbial infection can "break" a peripheral tolerance based on lymphocyte energy. Antibodies like human IgG1 and IgG3 are also called 'adaptive opsonins'. In response to signalling by this second-signal receptor. List two of such changes and explain HOW each change enhances the immune response. Explain why only antibodies produced by T-dependent immune response can be used by effector cells like macrophages. and the ligand and receptor of the second system. 1 answers submitted. Which molecular process must have occurred in B cells? Which type of receptor is required on the surface of the effector cells? 0 answers submitted. Describe one set of conditions that will induce tolerance through a peripheral process where selfantigen interacts with T or B lymphocytes. (1) Explain which process is stimulated by this type of opsonin. together with the TcR primary signal. Chapters 8 & 9 1. mast cells and NK cells. (3) Describe which receptor(s) these cells have that are required. B7 on the macrophage as APC cell is the induced ligand for a confirmatory. Gamma-interferon induces in macrophages changes in differentiation and gene expression that play no direct role in activating phagocytosis but that activate the capability of macrophages in CMI responses. Chapters 5 & 6 1. eosinophils. (2) Identify the name(s) of the typical effector cells(s). 2 answers submitted. Lecture 8 – Immunology Online Questions. an additional second-signal system becomes active that confirms to the APC cell that continued changes in cell differentiation are proper. Identify the name (or names) of the cell on which B7 exists or is induced. 0 answers submitted Compilation of my favorite Waterborg replies to answers:  You ptalk about a lot but you answer neither question! . 0 answers submitted. (4) List consequences of activation of the receptor(s). cannot be compromised by a microbial infection. and the cell name(s) for the membrane-anchored components of the second signaling system. 3. 1 answers submitted. Also explain why central tolerance to self-antigens. Lecture 9 – Immunology Online Questions. Chapters 6 & 7 1.0 answers submitted. Lecture 11 – Immunology Online Questions. Name the receptor for the B7 ligand. 4.

which neutralizes microbes and toxins and does not allow them to bind to the Fc receptors on the macrophage. you can’t view it on the webpage. Enjoy your weekends! . at the infected tissue. You answered the question in a way that was not asked… this answer.not that I don’t think most people did this…) Answer is OK.) You apparently do not know what is meant by a paratope "reservoir"…. spelling is PROTEIN.. at least take the time to use the King’s English spelling of the words. it’s there . This type of question is very easy to change into a multiple-choice format !! Your statement "Class I MHC molecules express CD8 which are capable of becoming CTLs on activation. and good luck. It’s also funny that as a person who can’t say the word “three. not 'protien'. The statement "IL-4 blocks the phagocytic pathway by simulating the production of IgG4. ." does not make sense. after he corrected 5 people for using the French spellings of words. Note. My advice to you: understand what you write before you write anything otherwise nothing is right. Don’t waste too much time studying for this exam. ." make no sense at all!!! Good (although "responSe" is the English word to use) (Editor’s note: if you are going to plagiarize the book. (Editor’s note: you’d think he would have caught on to the plagiarization. would have been also completely invalid.                   Small correction: the receptors are TOLL-like. The sentences following ".” and misspelled many words in his own replies. If those who submitted answers to the questions that were not fully answered (and therefore not able to be seen and copied by me) would submit their answers and comments from Waterborg.. They are not troll-like! You 'almost' give the WHY answer… You give way too much detail!!! A lot is wrong with this answer… You do not answer the question asked." is nonsense. How can the two last sentences be true at the same time??? You are obviously a complete fool! You should run back to your daddy and cry on his front porch and beg him to let you come back home! (Editor’s note: this was a response to one of my own answers. he would correct someone else’s grammar – see his next 2 grade replies. See my responses to other. I’m sure it would be beneficial to many! Thanks.) Very goof You ptalk about a lot but you answer neither question! OK…but The italicized sentences do NOT give any part of the answer requested! I have to take exception to the statement “…. and the word you mistreat multiple times is spelled "vesicle". as you interpreted it. but since not enough people submitted questions for that one. You’ll have to trust me. better answers. OK.