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Patho- Immunity

First Line of Defense: Surface Defenses

Physical & mechanical barriers
o Fast & non-specific response
o Skin
o Mucous membrane linings of the GI, GU, and respiratory tracts work
to repel invaders
Sloughing off of cells
Coughing, sneezing
Mucus & cilia- protective role against invaders
Biochemical barriers
o Synthesized & secreted saliva, tears, earwax, mucous, sweat, &
o Characterized by antimicrobial peptides
Cathelicidin, defensins, & collectins [skipped these]
o Normal bacterial flora- role is significant as first line
Second Line of Defense: Inflammation
Inflammatory response
o Often called innate/natural immunity
o Fast & non-specific response
o Begins within seconds of injury or invasion
o A vascular response that surrounds affected tissues with cells & fluids
Isolate, destroy, and remove invaders
Promote healing read about tissue reapir in text****
Local Manifestations of Inflammation look for these as NP in all pts
o Erythema
o Edema
o Heat
o Pain
o Loss of function (bc it hurts)
Systemic Manifestations of Inflammation
o Fever [skipped]
Caused by exogenous and endogenous pyrogens
Acts directly on hypothalamus
o Leukocytosis
Increased # of circulating leukocytes
o Increased plasma protein synthesis order these labs as NP if
suspect inflammation that is insidious to assess inflammatory process
Acute-phase reactants
C-reactive protein, fibrinogen, haptoglobin, amyloid,
ceruloplasmin, etc.

Increased ESR

Third Line of Defense: Immunity

Immunity- adaptive immunity (not innate)
Slow & specific response involving:
o B Lymphocytes
Part of humoral response
Antibodies in the blood (humor)
o T Lymphocytes
Cell mediated response
Various types of T cells: cytotoxic, helper, regulatory, etc.
o Other cells
Dendritic cells
Natural killer cells
Overview of Adaptive Immunity
Works together w/ inflammation
Recognizes foreign or non-self substances
o Antigens
Non-infectious environmental agents
Provides long-term protection to host (human body)
Slower than innate but more specific
Has memory*
Overview of Adaptive Immunity
End products
o Lymphocytes: T & B cells
o Antibodies: Immunoglobulins (Ig)
Generation of clonal diversity
o Each individual T or B cell specifically recognizes only one particular
o Sum of population of lymphocyte specificities may represent millions
of foreign antigens
o Primary lymphoid organs: thymus for T cells and bone marrow for B
Overview of Adaptive Immunity
Clonal diversity
o Occurs in primary lymphoid organs [thymus & bone marrow]
o Involves the maturing of B & T cells

o Migrates to secondary lymphoid organs

Clonal selection
o Antigen is processed & presented to immune cells by antigenpresenting cells (APCs)
Results in the differentiation of B cells into active antibodyproducing cells (plasma cells) and T cells into effector cells

Humoral & Cell-Mediated Immunity

Humoral immunity
o B cells & circulating antibodies are the primary cells
o Causes direct inactivation of a microorganism or the activation of
inflammatory mediators
o Primarily protects against bacteria & viruses
Cell-mediated immunity
o Differentiates T cells
o Primarily protects against viruses & cancer
Humoral & cellular immunity work together to provide immunity & memory
o Respond more rapidly & efficiently on subsequent exposure to the
same antigen
Type of


Primary Cells
B cells &
T cells

Causes direct inactivation of
a microorganism or the
activation of inflammatory
T-cell differentiation

Protects against
bacteria and viruses
Protects against
viruses and cancer

Kills targets directly, or

stimulates the activity of
other leukocytes
Active Immunity- Active Acquired
Antibodies or T cells are produced
after either a natural exposure to an
antigen or after immunization
Is long lived

Passive Immunity- Passive Acquired

Preformed antibodies or T lymphocytes
are transferred from a donor to a
Occurs naturally or artificially
Is temporary or short lived
Ex. breast milk

A molecule that can react with antibodies or receptors on B & T cells
Mostly protein but can be other molecules as well
Immunogenic antigen: an antigen that can trigger an immune response
Sites for binding to antibodies & lymphocytes

o Antigens binding site: antigenic determinant (epitope)

o Antibody or lymphocytes binding site: antigen-binding site (paratope)
Degree to which an antigen has immunogenic capability
o Degree of foreignness to a host most important
o Size
Large- extremely immunogenic
Small- molecular weight antigens are called haptens: cant
trigger the immune response themselves but can when bound
to a carrier protein
o Chemical complexity- the greater the diversity, the more the
o Amount- high or low extremes can cause tolerance dose is

MHC- Major histocompatibility complex

Most antibody and cellular immune responses are dependent on antigen
presentation by APCs MHC play a role in presenting the antigen to
the T cell
Glycoproteins that are found on the surface of all human cells (except RBCs)
Synonym Human leukocyte antigens (HLA) alleles: inherited in a codominant fashion to enable both maternal & paternal antigens to be
MHC class I genes: A, B, C
MHC class II genes: DR, DP, DQ
MHC class III genes: other genes that control the quality & quantity of an
immune response
Cells in transplanted tissue from one individual have a different set of MHC
surface antigens than those of the recipient
Recipient can mount an immune response against foreign MHC molecules
The more similar two individuals are in HLA tissue type, the more likely for a
successful transplant helps avoid rejection
Haplotype: a specific combination of alleles at the 6 major HLA loci on one
chromosome (A, B, C, DR, DQ, and DP)
Molecules That Recognize Antigens
o Circulating antibody
o Antigen receptors on B cells or can call them B-cell receptors (BCR)
o Antigen receptors on T lymphocytes or T-cell receptors (TCR)
T-Cell Maturation
Thymus is the central lymphoid organ of T-cell development
Shrinks after 1st year of life, by old age only about 15% of original size

T cells move from the thymic cortex to the medulla

Changes include development of the TCRs and the expression of surface
T cells are released into the blood & take up residence in the secondary
lymph organs to await antigens

T-Cell Activation
Initiates cellular immune response
Binds antigens to TCRs
o Direct killing of foreign or abnormal cells (Tc cells or cytotoxic T
lymphocytes [CTLs])
o Assistance or activation of other cells
T-regulatory cells (Treg)
o Regulate the immune response to avoid attacking self
T-memory cells
Activation = a series of Cellular interactions
o Recognize antigen that has been processed and presented by MHC
class I molecules or CD8 T cells are class I restricted
o Appropriate signaling pathways are needed for the maturation of T
B7 on the cell-presenting antigen
CD28 on the T cell
Cd48 on the APC
CD2 on the T cell
Variety of other adhesion molecules
Requires cytokines, especially IL-2, produced by the Th-1 cell
Cellular differentiation
o Produces active Tc cells with the capacity to identify antigens on the
surface of infected or malignant cells and then to destroy these cells
o Produces memory T cells
Have the capacity to respond rapidly if further exposure to the
same antigen occurs
Helper T cells assist with antigen presentation
B-Cell Maturation
Occurs in bone marrow
Stem cell matures & develops surface markers [skipped rest]
o CD45R and the interleukin (IL)-7 receptor
IL-7: produced by stromal cells
Critical in driving the further differentiation & proliferation
of the B cell
Production of BCRs [skipped]
o Heavy & light chains
o V, D, and J genes

Central Tolerance
Large number of auto-reactive B cells are eliminated if exposed to self
antigenover 90%
Concept of not attacking cells
B-Cell Activation
Results from the recognition of soluble antigen by BCReceptors, processing
of antigen, and presentation by MHC class II antigens to Thelper2 cells
When an immunocompetent B cell encounters an antigen for the first time,
B cells with specific BCRs are stimulated to differentiate and proliferate
A differentiated B cell becomes a plasma cell***
Plasma cell is a factory for antibody production
o May be a single class or subclass of a specific antibody
Secondary Lymphoid Organs
Lymph nodes
Peyer patches (intestines)
T Lymphocytes
Generated from immature precursors in thymus
o Originate from PPSC in bone marrow
o Differentiate into the lymphoid stem cell
o Processed through thymus gland
o Thymocytes- T cell precursors
Mature, T cells are found****
o In the blood, constituting 60-70% of lymphocytes
In T-cell zones of peripheral lymphoid organs, such as the
paracortical areas of lymph nodes, and periarteriolar sheaths of
the spleen
Each T cell is genetically programmed to recognize a specific cell-bound
antigen by means of an antigen-specific T-cell receptor (TCR)
The TCR recognizes antigens that are displayed by molecules on surfaces of
antigen-presenting cells
T cells (in contrast to B cells) cant be activated by soluble antigens
Presentation of processed antigens by antigen-presenting cells
(macrophages, dendritic cells) is required for induction of cell-mediated
T Lymphocytes Continued

Most of the T cells in body belong to one of 2 subsets, distinguished by the

presence on their surface of one or the other of two glycoproteins
o CD4
o CD8

T Lymphocytes Continued
CD4+ T cells
o Essential for both cell-mediated and antibody-mediated of
immune system
Cell-mediated immunity
o These CD4+ cells bind to antigen presented by antigen-presenting
cells (APCs) like phagocytic macrophages & dendritic cells
o T cells then release lymphokines that attract other cells to the area
Result is inflammation: the accumulation of cells & molecules
that attempt to wall off & destroy the antigenic material
Ex. abscess, rash after poison ivy
Antibody-mediated immunity
o These CD4+ cells, called helper T cells, bind to antigen presented by
B cells
o Result is the development of clones of plasma cells secreting
antibodies against the antigenic material
o CD4 cells main role = helper cell**
o CD-4 cells facilitate both inflammation & antibody responses
CD8+ cells or killer T cells
o Cytotoxic T Cell (Tc)
Kill cancer cells
Kill cells infected with a virus
CD8+ cells secrete molecules that destroy the cell to which
they have bound
Regulatory T cells (Tregs)
o Shut down immune system after invading organisms have been
eliminated - so doesnt continue regulated

CD4-CD8 Cells
There is some disagreement about the normal range for CD4 and CD8 cell
o Normal CD4 counts between 500-1600
o Normal CD8 counts between 375-1100
CD4 counts drop dramatically in people with HIV- in some cases down to
The ratio of CD4 cells to CD8 cells is often reported
o Calculated by dividing CD4 value by the CD8 value
o Normal: ratio between 0.9-1.9
Meaning there are about 1 to 2 CD4 cells for every CD8 cell [in
a normal physiologic situation]
But common for more CD8 than 4 in certain diseases
Dendritic Cells
Originate from hematopoietic stem cells in the bone marrow
o Myeloid stem cell
Precursors - monocytes/macrophages, granulocytesneutrophils/eosinophils, thrombocytes, basophils/mast cells,
dendritic cells, & erythrocytes
o Lymphoid stem cell
Seem to be also derived from lymphoid precursors
Found in the lymph nodes & spleen
Engulf pathogens & degrade them into protein fragments*****

o Display the protein fragments from the degraded pathogens on their

cell membranes
o One of most effective APCs in immune system!
o B-cells & T-cells
Recognize proteins & protein fragments, (antigens), and launch
a potent antigen-specific immune response
Thus, dendritic cells are known as antigen-presenting cells

Natural Killer (NK) Cells

Type of cytotoxic lymphocyte
Function = to recognize & eliminate cells infected with viruses
Some function in eliminating cancer cells
Part of the mononuclear phagocyte system
Have an important critical role in inflammation
Play important roles in the induction & effector phase of immune responses
(the sounds alarm)
Macrophages that have phagocytosed microbes & protein antigens
o Process the antigens
o Present peptide fragments to T cells
o Induces the cell-mediated immunity
Macrophages are important effector cells in certain forms of cell-mediated
immunity, such as delayed hypersensitivity reactions*
Are activated by cytokines
o Notably substances produced by the TH1 subset of CD4+ cells
Important in the effector phase of humoral immunity
Phagocytose microbes that are opsonized by IgG or C3b [skipped]
Identification of Self vs. Non-self A Review Slide
o Proteins on the surface of all cells in the body (except RBCs) that
distinguish an individuals cells from the cells of another (SELF VS.
o Non-self antigens, infectious agents, non-infectious agents from the
environment, drugs & vaccines, transfusions & transplanted tissues
Immune Response
o Bodys response to antigenic challenges
o Maturation & activation of lymphocytes
o B lymphocytes mature to be plasma cells
Produces antibodies to incapacitate the antigen
Against specific antigens
Memory cells produced
o T lymphocytes
Attack antigen directly

Against specific antigens

Memory cells
o Immune response has memory & specificity
Antibody development
B lymphocytes mature to be a plasma cell, which is a factory for antibody
o Single class or subclass of antibody
Plasma cells secrete immunoglobulins
Immunoglobulins with specificity are antibodies
Also called immunoglobulin (Ig)
Produced by plasma cells
Has several classes characterized by antigenic, structural, and functional
o IgA
Found predominantly in body secretions
Secretory (mucosal) immune system
Lymphoid tissues that protect the external surfaces of the
Antibodies present in tears, sweat, saliva, mucus, and
break milk
IgA = dominant immunoglobulin
Small numbers of IgG and IgM present
Can pass passive immunity through breastfeeding
o IgM
Largest number of immunoglobulins
First antibody produced during the primary response to an
Significant antibody produced during a secondary response
Synthesized during fetal life
Large & early arriver
o IgG
Most abundant class (80-85%)
Gamma globulin
Transported across the placenta**
Four classes: IgG1, IgG2, IgG3, IgG4
o IgE
Least concentrated of the immunoglobulin classes in the
Mediator of many common allergic responses
Defender against parasites
Eosinophils are a partner
o IgD


Limited info on function

Low concentration in blood
Located primarily on surface of developing B lymphocytes
Function as one type of B cell antigen receptor

Most prevalent,
-Most of
activity against
-Crosses the

Mostly in
-Most of
activity in

Most rare
-Mediator of
many common
-Defends against

Not well
Functions as
one type of

Largest #
First antibody
during the
initial, or
response to an
-Large & early

Antibody Function
Directly through:
o Neutralization
o Agglutination
o Precipitation
Indirectly through:
o Opsonization
Degree of antibody protection is assessed by an antibody titer
o Prove when given immunization in past or when had infection
Primary and Secondary Responses
Primary response
o Initial exposure
o Latent period or lag phase
B cell differentiation is occurring
o After 5-7 days, an IgM antibody for a specific antigen is detected
o An IgG response equal or slightly less follows the IgM response
Secondary response
o More rapid
o Larger amounts of antibody are produced
o Rapidity due to presence of memory cells that do not have to
o IgM is produced in similar quantities to the primary response, but IgG
is produced in considerably greater numbers


Natural vs. Acquired Immunity

Natural Immunity (native/innate resistance)
o Present at birth
o Not produced by hosts immune response
o Species dependent
o Host dependent
o Fast, non-specific
Acquired Immunity
o Gained after birth
o Active acquired: produced by host after antigen exposure
Naturally (or accidental exposure to an antigen)
Immunization with biological material
o Passive acquired: does not involve the hosts immune response
Maternal antibodies
Immunization with preformed antibodies
Altered immunologic response to an antigen that results in disease or
damage to the host
o Allergy
Exaggerated immune response to non-self
o Autoimmunity
Misdirected immune response against self
o Alloimmunity
Normal immune reaction against beneficial foreign tissue
Exaggerated immune response to non-self exogenous antigens
Allergens are environmental antigens that cause atypical exaggerated
immunologic responses in genetically predisposed individuals
o Environmental allergens

Molds, fungus
Cigarette smoke
Household dust
o Drug allergens (penicillins)
o Haptens- antigens reacting with skin self-proteins
Metals (nickel)
Chemicals (rubber)
Resins (poison ivy, poison oak)
o Allergen is contained within a particle too large to be phagocytosed or
is protected by a nonallergenic coat
Immunologic Tolerance
Immune tolerance is the phenomenon of unresponsiveness to an antigen
induced by exposure of lymphocytes to that antigen
Self tolerance refers to the lack of responsiveness to an individuals own
Lymphocytes with receptors capable of recognizing self antigens are
generated constantly, and these cells must be eliminated or inactivated to
prevent them from causing harm
Mechanisms of self-tolerance
o Central tolerance
Immature, self reactive T & B lymphocytes clones that
recognize self antigens during their maturation in the central
lymphoid tissues (thymus & bone marrow) are killed or
rendered harmless
Negative selection or deletionT cells
Self-reactive lymphocytes are eliminated from the T-cell
Receptor EditingB cells
25-50% of B cells undergo receptor editing during their
maturation process
o Peripheral tolerance
Central tolerance is imperfect; back up system is peripheral
Some mechanisms:
o Lymphocytes that recognize self antigens may be
rendered functionally unresponsive
Suppression by tregs
Deletion by apoptosis
o Cells that recognize self antigens may receive
signals to promote apoptosis

Misdirected immune response against self antigens
o Genetic susceptibility
Twin studies
Association of HLA alleles
Lessons from genome wide studies
o Environmental triggers
o Role of infections
As triggers?
As protective?
Also called isoimmunity
Normal immune response against beneficial foreign tissue
Immune system reacts with antigens on the tissue of other genetically
dissimilar members of the same species
Transient neonatal alloimmunity
o Fetal antigens cross placenta
o Mother makes antibodies
o Antibodies cross placenta and cause disease
Transplant rejection and transfusion reactions
Responses after re-exposure to an antigen
o Immediate
Occurs within minutes
If severe, called anaphylaxis described below
o Delayed
Takes several hours to appear
Maximum severity days after exposure
o Anaphylaxis
Most rapid and severe immediate response that occurs within
Typically systemic (generalized)
Itching & erythema
Abd cramps
Breathing difficulties & laryngeal edema
Vascular collapse & hypotension
Anaphylactic shock & death
Characterized by the immune mechanism

o Type

o Type

o Type

o Type

IgE mediated
Tissue-specific reactions
Immune complex mediated
Cell mediated

Type I Hypersensitivity
Most common allergic reactions
o Antibody mediated
o Initial sensitization to an allergen
o B cell stimulated to produce IgE
o IgE coats mast cell surface
o Further exposure to same allergen cross-links the surface bound IgE
and causes mast cell degranulation
o Histamine release
Genetic predisposition = atopic
o Food challenges
o Skin tests- wheal & flare reaction
o IgG-blocking antibodies
Type I Examples
o Common allergic reactions
o Extrinsic asthma
o Others
Type II Hypersensitivity
Tissue specific
o Specific cell or tissue (tissue-specific antigens) is the target of an
immune response
o Antibody mediated
Five mechanisms


Type II Examples
o Hemolytic anemia
o Graves disease
Autoimmune thyroiditis
o Myasthenia Gravis
Post synaptic acetylcholine receptors
o Others

Type III Hypersensitivity

Immune complex mediated
Antigen-antibody complexes are formed in the circulation and are later
deposited in vessel walls or extravascular tissues
Not organ specific
Immune complex clearance
o Large macrophages
o Small renal clearance
o Intermediate deposit in tissues
Type III Examples
o Acute serum sickness
A sysetmic immune complex disease
It was at one time a frequent sequela to the administration of
large amounts of foreign serum

(ex. immune serum from horses used for passive

o The occurrence of diseases caused by immune complexes was
suspected in the early 1900s by a physician named Clemens von
o In modern times the disease is infrequent, but it is an informative
model that has taught us a great deal about systemic immune
complex disorders
Seen with the use of ATG
Serum Sickness Examples
Following Antithymocyte Globulin (ATGAM) infusion
The incidence of fever, skin rashes, and arthralgia is believed to represent
serum sickness
Occur 7-10 days after administration or 1-2 days with repeated
Treatment with corticosteroids
Arthus Reaction
Discovered by Arthus in 1903
o Arthus repeatedly injected horse serum subcutaneously into rabbits
o Sometimes after vaccination: tetanus toxoid-containing or diphtheria
toxoid-containing vaccines
o Heparin, bee sting
Local vasculitis associated with deposition of immune complexes and
activation of complement
High local concentration of vaccine antigens and high circulating antibody
Severe pain, swelling, induration, edema, hemorrhage
Signs & symptoms occur 4-12 hours after vaccination
Type III Hypersensitivity Examples
Raynauds phenomenon
o Temperature dependent vasospasm of digits/peripheral circulation
o May be caused by immune complex deposition
Systemic Lupus Erythematous (SLE)
o Classic Type III hypersensitivity disorder
Type IV Hypersensitivity
Does not involve antibody as primary mechanism
Cytotoxic T lymphocytes or lymphokine producing Th1 cells
o Direct killing by Tc or recruitment of phagocytic cells by Th1 cells
o Acute graft/transplant rejection

o Skin rest for TB

o Contact allergic reactions
o Some autoimmune diseases like Type 1 diabetes, Hashimotos
Additional Examples of Type I, II, III, IV
Type I
o Extrinsic asthma
o From the Greek meaning gasp
o Common chronic inflammatory disease of the airways characterized
by variable and recurring symptoms, airflow obstruction, and
o Caused by exaggerated immune response to exogenous antigens
o Symptoms include wheezing, coughing, chest tightness, and SOB
o Symptoms can be prevented by avoiding triggering such as allergens
and irritants and by pharmacologic manipulation
Beta 2 agonist and corticosteroids
Anti-inflammatory medications

Type II disorder: ITP

o Immune thrombocytopenic purpura (ITP)
Decreased number of circulating platelets (thrombocytopenia)
Manifests as a bleeding tendency, easy bruising (purpura), or
extravasation of blood from capillaries into skin and mucous
membranes (petechiae)
o Platelets are coated with autoantibodies to platelet membrane
antigens, resulting in splenic sequestration and phagocytosis by
mononuclear macrophages
o The resulting shortened life span of platelets in the circulation,
together with incomplete compensation by increased platelet
production by bone marrow megakaryocytes, results in decreased
platelet count
o Autoantibody stimulation
Membrane GPs on the surface of platelets become
immunogenic, stimulating the production of platelet
The stimulus for autoantibody production is unknown
Platelet membrane cryptantigens may become exposed by the
stress of infection, or pseudoantigens may be formed by the
passive adsorption of pathogens on platelet surfaces
o Role of the spleen
Spleen is site of autoantibody production (white pulp)
Also site of phagocytosis of autoantibody-coated platelets (red
o Platelet destruction


The mononuclear macrophage system of the spleen is

responsible for removing platelets in immune thrombocytopenic
purpura (ITP), because splenectomy results in prompt
restoration of normal platelet counts in most patients with
immune thrombocytopenic purpura (ITP)
o Morphology
Decreased platelet count
Enlarged spleen
o Clinical Manifestations
Bleeding manifestations
o Treatment
Splenectomy if medications do not work

Type III: Systemic Lupus Erythematous (SLE)

o Patho
Chronic multisystem inflammatory disease
Autoantibodies against:
Nucleic acids, erythrocytes, coagulation proteins,
phospholipids, lymphocytes, platelets, etc.
Deposition of circulating immune complexes containing
antibody against host DNA
The classic Type III hypersensitivity disorder
Diverse deposition
More common in females
Characterized by exacerbations & remissions
o Clinical Manifestations
Arthralgias or arthritis (90% of individuals)
Vasculitis and rash (70-80%)
Renal disease (40-50%)
Hematologic changes (50%)
Cardiovascular disease (30-50%)
o Serial or simultaneous presence of at least four of the eleven common
findings indicates SLE diagnosis
Facial rash (malar rash), discoid rash, photosensitivity, oral or
nasopharyngeal ulcers, nonerosive arthritis, serositis, renal
disorder, neurologic disorder, hematologic disorders,
immunologic disorders, and presence of antinuclear antibodies
Malar rash: latin for cheek
o Butterfly rash
o Classic CM
Discoid rash
o Coin shaped or oval, like a disk, and seen on areas
of the skin that are exposed to sunlight

o Lesions (sores) tend to be red and raised and

become scaly. May leave scar after healed
o Rashes can also result in change in coloring of skin,
making the area around the lesion either lighter or
darker in color
o May appear on scalp, face in a butterfly distribution,
or I areas where the skin receives sun exposure
o Lesions are usually painless and typically do not itch
o SOAP BRAIN MD- useful mnemonic for the 11 criteria of SLE
Oral ulcers
Blood changes
Renal involvement (proteinuria or casts)
Immunological changes
Neurological signs (seizures, frank psychosis)
Malar rash
Discoid rash
o Morphology of SLE
+ Antinuclear antibody (ANA)
+ Lupus Erythematous Antibody (LE Prep)
Increased erythrocyte sedimentation rate (ESR)
o Treatment
Treat specific complications
Renal involvement
Vasculitis and HTN

Type IV: Graft Rejection

o Hyperacute
Immediate and rare
Preexisting antibodies
o Acute
Weeks after transplant- cell mediated immune response
Immunosuppressive drugs used to manage
o Chronic
After months or years of normal function
Slow progressive organ failure despite immunosuppressive drug
o Morphology

Biopsy of grafted tissue shows inflammatory damage

Transplanted tissue/organ dysfunction
o Clinical Manifestations
Signs of dysfunction/failure of transplanted tissue/organ
o Treatment
Antirejection medications
Graft v. Host Disease
Bone marrow transplant complication
Transplanted bone marrow
o More immunocompetent than the immunosuppressed host
Graft (transplanted BM) attacks the host
o Type IV hypersensitivity
o Inflammatory lesions
Treated with immunosuppressive medications
Immune disorders may involve several of these mechanisms
Latex allergy
Type I? or Type IV?
Which mechanisms are implicated?
Immune Deficiencies
Failure of immune mechanisms of self-defense
Congenital (primary)
o T or B cell lines may be deficient
Hypogammaglobulinemia- deficient immunoglobulins
Severe combines immune deficiencies (SCIDS)
DoGeorge syndrome- congenital thymic aplasia/hypoplasia
Acquired (secondary)
o Caused by another illness
Viral illness (HIV)
Normal physiologic changes of aging
Nutritional deficiency
Iatrogenic deficiency (drugs/treatment)
Burn victims
Deficiency caused by stress
Classic Clinical Presentation
o Opportunistic infections
Unusual or recurrent, severe infections that immunocompetent
individuals do not develop (Not normally pathogenic)
o Pneumocystis carnii pheumoia (PCP)

o Cytomegalobirus (CMV)
o Herpes virus
o Mycobacterium avium intracellulare (MAI)
o others
Fungi and yeasts