IMMUNOLOGY

IL4 and IL5 secreted by Th cells stimulates B cells to become plasma cell and secrete antibodies

IL2 activates Tc cells

Defensins. These are highly positively charged (cationic) peptides that create

pores in the membranes of bacteria, which kills them, Alpha defensin- intestines, Beta defensin -
respiratory tract

acute-phase response, are also produced early in inflammation, mainly by the liver. The best known
of these are C-reactive protein

and mannose-binding protein, which bind to the surface of bacteria and enhance the activation of
the alternative pathway of complement

Gamma interferon, which activates macrophages and enhances their microbicidal action, is
produced by activated helper T cells.

Macrophages are principal source for IL6 which is pro-inflammatory

Interleukin-8 is a chemokine that attracts primarily neutrophils, whereas monocyte chemotactic

protein 1 (MCP-1) and macrophage inflammatory protein (MIP) are attractants for macrophages and
monocytes

The C5a component of complement is another important chemokine

in typhoid fever leukopenia is seen

Migration of PMNs to the infection site is due to the production of chemokines, such as interleukin-8
and complement component C5a, at that location.

LFA proteins,” located on the PMN surface, with intracellular adhesion molecule (ICAM) proteins on
the endothelial cell surface.

during an infection the ICAMs are increased from stimulation by IL1 and TNF from macrophages
The outer cell membranes of both PMNs and macrophages have receptors both for the Fc portion of
IgG and for C3b and these are the major opsonizers

neutrophil function is reduced in episode of diabetic ketoacidosis

interferon gamma is important for macrophage activation

certain antigens (e.g., bacterial polysaccharides) can activate B cells directly, without the help of T
cells, and are called T-cell–independent antigens. In this T-cell– independent response, only IgM is
produced by B cells

because it requires IL-4 and IL-5 made by the helper T cell for the B cell to “class switch” to produce
IgG, IgA, and IgE.

The macrophage makes interleukin(IL)-1, which helps activate the CD4 cell. The activated CD4 cell
makes interleukins (e.g., IL-2, which activates the CD8 cell to attack the virus infected

cell, and IL-4 and IL-5, which activate the B cell to produce antibody).

IgM receptors located on B cells are also virus specific. IgM antigen receptor on the B cell can
recognize not only foreign proteins but also carbohydrates, lipids, DNA, RNA, and other types of
molecules. The class II MHC proteins

of the B cell, however, can only present peptide fragments to the helper T cells.

children with severe combined immunodeficiency disease (SCID), who have intact innate immunity
but no adaptive immunity, suffer from repeated, life-threatening infections.

(NOD receptors and RIG-I helicase receptors) that recognize microbes within cells.

There are two classes of receptors on the surface of cells (Toll-like receptors and mannan-binding
lectin receptors) that recognize microbes outside of cells

APOBEC3G (apolipoprotein B RNA-editing enzyme) Causes hypermutation in retroviral DNA and

mRNA

humoral (antibody-mediated) response is produced against one type of bacteria, but a cell-mediated
response occurs in response to a different type of bacteria. The process that
determines the type of response depends on the cytokines produced by the macrophages, and this
in turn depends on which pattern-recognition receptor is activated by the organism,

LPS-binding protein, a normal component of plasma. This binding protein transfers LPS to a receptor
on the surface of macrophages called CD14. LPS stimulates

a pattern-recognition receptor called Toll-like receptor 4 (TLR4), which transmits a signal, via several
intermediates, to the nucleus of the cell. This induces the production of

cytokines, such as IL-1, IL-6, IL-8, and tumor necrosis factor (TNF), and induces the costimulatory
protein, B7, which is required to activate helper T cells and to produce antibodies.

TLR4-Gram negative bacteria

TLR2-GRAM POSITIVE bacteria, yeasts

mannose binding lectins activates complement

NOD receptors recognise bacterial peptidoglycan within the cytoplasm imp to fight intracellular
pathogens

RIG-I helicase receptors recognize the nucleic acids of viruses in the cytoplasm of infected cells

The acute-phase response, which consists of an increase in the levels of various plasma proteins
(e.g., C-reactive protein and mannose-binding protein), is an important

part of innate immunity. These proteins are synthesized by the liver and are nonspecific responses to
microorganisms and other forms of tissue injury

these are synthesized in response to IL1, IL6 and TNF from macrophages

IL1 IL6 are pro inflammatory cytokines

IL10 , TGF BETA are anti inflammatory

α-Defensins also have antiviral activity. They interfere with human immunodeficiency virus (HIV) binding to
the CXCR4 receptor and block entry of the virus into the cell.
HIV has developed VIF (viral infectivity protein) to deal with this.

Alpha and beta interferons are important antiviral proteins.

Gamma interferon is an important mediator of inflammation but has only modest antiviral activity. It acts
primarily to enhance killing by macrophages and other phagocytes, and to increase the synthesis of class 1 and
class 2 MHC proteins.

drugs (e.g., penicillin) and poison oak oil, bind to our normal proteins, to which we are tolerant. The hapten–
protein combination now becomes immunogenic (i.e., the hapten modifies the protein sufficiently
such that when the hapten–peptide combination is presented by the MHC protein, it is recognized as
foreign).
conjugate vaccines such as the pneumococcal and meningococcal vaccines and the vaccine against
Haemophilus influenzae. In these conjugate vaccines, the capsular polysaccharide is conjugated to a carrier
protein. The capsular polysaccharide is not a hapten because it can induce IgM via the T-independent response.
However, adding a carrier proteincauses helper T cells to be involved, and large amounts of IgG are produced
via the T-dependent response.

how a univalent hapten, such as penicillin, causes anaphylaxis??

Sufficient penicillin binds to one of our proteins to cross-link IgE.

adjuvant is not covalently bound to the immunogen, whereas the carrier protein is.

pneumococcal vaccine containing the unconjugated polysaccharides does not induce protective immunity
when given prior to 18 months of age, but the pneumococcal vaccine containing the polysaccharides conjugated
to a carrier protein is effective when given as early as 2 months of age. This indicates the children under the age
of two years do not mount a protective T-independent response

formation of T cells and B cells from stem cells is enhanced by interleukin-7 (IL-7)

The double-negative cells and the double-positive cells are located in the cortex of the thymus, whereas the
single-positive cells are located in the medulla.
Double +: having both CD3 and CD4

A transcriptional regulator called the autoimmune regulator (AIRE) enhances the synthesis of this array of
self-proteins. Mutations in the gene encoding the AIRE protein results in the development of an autoimmune
disease called autoimmune polyendocrinopathy.

Thymic education processes produce T cells that are selected for their ability to react both with foreign antigens
via their antigen receptors and with self MHC proteins.

receptor editing. In this process, a new, different light chain is produced that changes the specificity of the
receptor so that it no longer recognizes a self-protein. It is estimated that as many as 50% of self-reactive B cells
undergo receptor editing. T cells do not undergo receptor editing

NK cells target those cells to be killed by detecting that they do not display class I MHC proteins on the cell
surface.