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MHC
present on every nucleated cell of body. Class I and class II are called HLA molecules (human leukocyte antigens)

Class I: "self" antigens.

Class II: invader antigens.
IgG
85% of circulating immunoglobulin

Found in serum, across placenta. Activated complement, macrophages, neutrophils and platelets. Can cause agglutination and precipitation. 2ndry response.
IgA
15%. Found in serum, GI, colostrum, tears, sweat, urine, lungs. Activates complement. To guard the linings to outside of body.
IgM
6-10%. Serum. Immature B cells synthesize. Primary response.
IgD
Serum. B cell plasma membrane in conjunction with IgM. Marks a mature B cell.  **No complement activation.
IgE
least concentrated. Allergic response. Defense against parasitic invasions.
Generation of Clonal Diversity

vs.

Clonal Selection
Process by which immunocompetent B and T cells are made ready (generation of clonal diversity) and then customized to attack a particular antigen.

Generation of Clonal Diversity happens in primary  lymphoid organs (thymus and bone marrow) while Clonal Selection happens in 2ndry lymphoid organs (spleen, lymph nodes, adenoids, tonsils, Peyer's patches).
CD4

vs.

CD8
Helper T cells

vs.

Cytotoxic T cells
Type I hypersensitivity (incl. atopic)

process, function, details
- IgE mediated hypersensitivity

-anaphylaxis or allergic hypersensitivity (bee sting, allergic rhinitis, allergic asthma)

-IgE and mast cells. Fc complex on mast cell binds 2 IgE antibodies which then bind to allergen (which originally caused their production in the first place!) 

- environmental antigens (which are allergenic)

- early and late phases

-atopic: more IgE and more Fc receptors on mast cells. poor bastards.
Type II Hypersensitivity.

Process, examples, 5 processes
- Cytotoxic

- examples: transfusion reactions, Grave's Disease

- Antibody attacks a specific cell that presents an antigen on its cell surface

- Certain cells have these antigens, most done (e.g. RBCs, platelets, thyroid cells)

5 processes:
1. complement lysis (transfusion)
2. macrophage phagocytosis after opsonization (drug reaction to blood components)
3. complement mediated neutrophil damage
4. Antibody-dependent cell mediated cytotoxicity (ADCC) - NK cells
5. Antibody binding with malfunction of the cell (Grave's Disease, Myasthenia Gravis)
Type III Hypersensitivity
Immune Complex Disease:

ex: Local: farmers lung, arthus; Systemic: Serum sickness (e.g. raynaud phenomenon)

- The antibody binds to a soluble antigen in the blood and then precipitates and deposits into the tissue (usually of the venous system)

- Complement and chemotaxis of neutrophils are involved and you get many problems arising from that.
Type IV Hypersensitivity
Contact Sensitivity, Delayed Sensitivity

eg: PPD, organ rejection, graft reaction, poison oak/ivy

- Tc cell mediated.

- No antibody involvement.

- Catechol is hapten that combines with skin protein to become allergen
Active vs. Passive Immunity


Natural vs. Induced of each
Responding to environmental antigen produces active immunity.

Acquiring antibodies as a result of "donation" from mother to fetus.

Natural Active: typical mode
Induced Active: conferred by exposure to antigens to ward off disease (e.g. vaccines)

Natural Passive: mother to fetus
Induced Passive: conferred by exposure of antibodies to ward off disease.
Antibodies work because of...
FAB section of structure.
Precipitation vs. Agglutination
Formation of antigen-antibody structure that aren't soluble and precipitate

Formation of antigen-antibody insoluble structure on cell walls (e.g. blood transfusion rxns)
Antibodies effects, direct vs. indirect
Direct:
Agglutination
Precipitation
Neutralization (keep foreign cells from being able to bind to self cell walls)

Indirect:
Opsonization
Role of complement with acquired immunity?
Hellz yeah! It's activated by most antigen-antibody complexes
Systemic Lupus Erythematosus

Pathophysiology and common clinical manifestations
Immune complexes formed and deposited in heart, kidneys and skin that contain anti-DNA auto-antibodies are formed.

Common clinical manifestations:
inflammation (esp. heart, kidney and skin); skin rash and photosensitivity; arthritis; renal disease; hematologic abnormalities; vasculitis
Agammaglobinemia
Congenital.

- No plasma cell development

- X chromosome linked (males)

- Frequent infections in URI and lower RI.
Severe combined Immunodeficiency
deficiency of stem cell makes lack of mature T and B cells.

- symptoms appear within 6 months, usually leads to death within 1 year
DiGeorge Syndrome
T cell deficiency that results from failure of normal development of 3rd and 4th pharyngeal pouches.

Accompanied by lack of effective thymus and defects of heart and great vessels

- poor defense against fungal and viral infections
Selective IgA Deficiency
Unknown etiology

- sinus, lung and GI infections

-  2 - 3 times more common in atopic individuals

- individuals not sensitized to IgA (through breast milk, bovine milk, blood from mom) can have analphylaxis from transfused IgA
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