MICROBIOLOGY & IMMUNOLOGY

MICRO: Immunology

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Matching: Immunoglobulin Isotypes:
-?-(d) IgD Unclear function; found on the surface of many B cells & in serum
-?-(b) IgA Prevents attachment of bacteria & viruses to mucous membranes, does not fix complement; monomer or dimmer; found in secretions; picks up secretory component from epithelial cells before secretion
-?-(e) IgE Mediates immediate (type 1) hypersensitivity by inducing the release of mediators from mast cells & basophils when exposed to allergen; mediates immunity to worms; lowest concentration in serum
-?-(a) IgG Main antibody in 2° response; most abundant; fixes complement, crosses the placenta, opsonizes bacteria, neutralizes bacterial toxins & viruses
-?-(c) IgM Produced in the 1° response to an antigen; fixes complement but does not cross the placenta; antigen receptor on the surface of B cells; monomer or pentamer
(a) IgG (b) IgA (c) IgM (d) IgD (e) IgE
Ig epitopes:
-?-allotype differs among members of same species
-?-isotype common to a single class of Ig
-?-idiotype determined by antigen-binding site
MHC I antigen loading occurs in -?-RER (viral antigens) and MHC II antigen loading occurs in -?-acidified endosome.
Th1 cells (produce -?-IL-2 and γ-interferon) activate macrophages and -?-Tc cells; Th2 cells (produce IL-4 and IL-5) help -?-B cells make antibody.
Adjuvants are nonspecific -?-stimulators by themselves; they are given with a -?-weak immunogen to enhance response; human vaccines contain -?-aluminum hydroxide or lipid adjuvants.
Helper T cells have -?-CD4, which binds to MHC II on anatigen-presenting cells; cytotoxic T cells have -?-CD8, which binds to MHC I on virus-infected cells.
Self-reactive T cells become nonreactive without -?-costimulatory molecules; B cells also become -?-anergic, but tolerance is less complete than in T cells.
Matching: Important cytokines:
-?-(d) IL-4 Secreted by helper T cells; promotes growth of B cells; enhances the synthesis of IgE & IgG
-?-(h) TNF-α Secreted by macrophages; ↑ IL-2 receptor synthesis by helper T cells; ↑ B-cell proliferation; attracts & activates neutrophils
-?-(i) TNF-β Secreted by activated T lymphocytes; functions similar to those of TNF-Α
-?-(b) IL-2 Secreted by helper T cells; stimulates growth of helper & cytotoxic T cells
-?-(g) γ-interferon Secreted by helper T cells; stimulates macrophages
-?-(c) IL-3 Secreted by activated T cells; supports the growth & differentiation of bone marrow stem cells; has a function similar to GM-CSF
-?-(a) IL-1 Secreted by macrophages; stimulates T cells, B cells, neutrophils, fibroblasts, & epithelial cells to grow, differentiate or synthesize specific products; an endogenous pyrogen
-?-(e) IL-5 Secreted by helper T cells; promotes differentiation of B cells; enhances the synthesis of IgA; stimulates production & activation of eosinophils
-?-(f) IL-8 Major chemotactic factor for neutrophils
(a) IL-1 (b) IL-2 (c) IL-3 (d) IL-4 (e) IL-5 (f) IL-8 (g) Γ-interferon (h) TNF-Α (i) TNF-Β
Matching: cell surface proteins:
-?-(d) macrophages MHC II, CD14:
-?-(f) all cells except mature red cells MHC I:
-?-(a) helper T cells CD4, TCR, CD3, CD28:
-?-(c) B cells IgM, B7, CD19, CD20:
-?-(b) cytotoxic T cells CD8, TCR, CD3:
-?-(e) NK cells Receptors for MHC I, CD16:
(a) ) helper T cells (b) cytotoxic T cells (c) B cells (d) macrophages (e) NK cells (f) all cells except mature red cells
T-cell activation: foreign body is phagocytosed by -?-APC; foreign antigen is presented on MHC II and recognized by -?-TCR on Th cell; and, "costimulatory signal" is given by interaction of -?-B7 and CD28.
Complement defends against -?-gram-negative bacteria; activated by IgG or -?-IgM in the classic pathway; and, activated by toxins (including endotoxin), aggregated -?-IgA, or other conditions in the alternate pathway.
Interferons (Α,Β,Γ) are proteins that place uninfected cells in an -?-antiviral state; interferons induce production of a 2nd protein that inhibits viral -?-protein synthesis by degrading viral mRNA (but not host mRNA).
Matching: hypersensitivity
-?-(b) cytotoxic IgM, IgG bind to antigen on "enemy" cell, leading to lysis (by complement) or phagocytosis
-?-(a) anaphylactic & atopic Antigen cross-links IgE on presensitized mast cells & basophis, triggering release of vasoactive amines
-?-(e) arthus reaction A local subacute antibody-mediated hypersensitivity (type III) reaction; intradermal injection of antigen induces antibodies, which form antigen-anibody complexes in the skin
-?-(c) immune complex Antigen-antibody complexes activate complement, which attracts neutrophils; neutrophils Release lysosomal enzymes
-?-(f) delayed (cell-mediated) type Sensitized T lymphocytes encounter antigen & then release lymphokines (leads to macrophage Activation)
-?-(d) serum sickness An immune complex disease (type III) in which antibodies to the foreign proteins are produced (takes 5 days); immune complexes form & are deposited in membranes, where they fix complement (leads to tissue damage)
(a) anaphylactic & atopic (b) cytotoxic (c) immune complex (d) serum sickness (e) arthus reaction (f) delayed (cell-mediated) type

B-cell deficiencies:

Bruton's agammaglobulinemia deficiency: X-linked recessive defect in a tyrosine gene associated with low levels of all classes of: -?-immunoglobulins.

Selective immunoglobulin deficiency: Deficiency in a specific class of immunoglobins-possibly due to a defect in -?-isotype switching.

T-cell deficiencies:

thymic aplasia (DiGeorge syndrome): thymus & parathyroids fail to develop owing to failure of the development of the 3rd & 4th -?-pharyngeal pouches.

chronic mucocutaneous candidiasis: T-cell dysfunction specifically against -?-Candida albicans; presents with skin & mucous membrane

B- and T-cell deficiencies:

Severe combined immunodeficiency: defect in early stem-cell differentiation; presents with recurrent viral, bacterial, fungal, and -?-protozoal infections; may have multiple causes.

Wiskott-Aldrich syndrome: X-linked defect in the ability to mount an -?-IgM response to capsular polysaccharides of bacteriua.

Ataxia-telangiectasia: Defect in DNA repair enzymes with associated IgA deficiency; presents with -?-ataxia and telangiectasia.

Phagocytic deficiencies:

Chronic granulomatous disease: defect in phagocytosis of neutrophils owing to lack of -?-NADPH oxidase activity or similar enzymes.

Chédiak-Higashi disease: autosomal recessive; defect in microtubular function & lysosomal emptying of phagocytic; presents with recurrent -?-NADPH infections by staphylococci & streptococci.

Job's syndrome: failure of -?-γ-interferon production by helper T cells; neutrophils fail to respond to chemotactic stimuli.

Leukocyte adhesion deficiency syndrome: defect in -?-LFA-1 adhesion proteins on phagocytes; presents early in life with severe pyogenic infections.

Hyper-IgM syndrome: defect in CD40 ligand on CD4 T helper cells leads to inability to class switch; presents early in life with severe -?-pyogenic infections.

IL-12 receptor deficiency: presents with disseminated -?-mycobacterial infections.

Active immunity: induced after exposure to foreign -?-antigens; slow onset; long-lasting protection (memory).

Passive immunity: based on receiving performed -?-antibodies from another host; rapid onset; short life span of antibodies.

Match autoantibody with associated disorder:
-?-(g) anti-Scl-70 Scheroderma (diffuse)
-?-(l) antimicrosomal Hashimoto's thyroiditis
-?-(a) ANA (antinuclear antibodies) SLE
-?-(b) anti-dsDNA, anti-Smith Specific for SLE
-?-(k) anti-epithelial cell Pemphigus vulgaris
-?-(c) antihistone Drug-induced lupus
-?-(d) anti-IgG Rheumatoid arthritis
-?-(e) antineutrophil Vasculitis
-?-(f) anticentromere Schleroderma (CREST)
-?-(h) antimitochondrial 1° biliary cirrhosis
-?-(j) anti-basement membrane Goodpasture's syndrome
-?-(i) antigliadin Celiac disease
(a) ANA (b) anti-dsDNA, anti-Smith (c) antihistone (d) anti-IgG (e) antineutrophil (f) anticentromere (g) anti-Scl-70 (h) antimitochondrial (i) antigliadin (j) anti-basement membrane (k) anti-epithelial cell (l) antimicrosomal
Transplant rejection: Matching
-?-(d) graft-vs-host disease Grafted immunocompetent T cells profliferate in the irradiated immunocompromised host & reject cells with "foreign" proteins, resulting in severe organ dysfunction; major symptoms include a maculopapular rash, jaundice, hepatosplenomegaly & diarrhea
-?-(c) chronic rejection Antibody-mediated vascular damage (fibrinoid necrosis); occurs months to years after transplantation; irreversible
-?-(b) acute rejection Cell mediated due to cytotoxic T lymphocytes reacting against foreign MHCs; occurs weeks after transplantation; reversible with immunosuppressants such as cyclosporine & OKT3
-?-(a) hyperacute rejection Antibody mediated due to the presence of preformed anti-donor antiboidies in the transplant recipient; occurs within minutes after transplantation
(a) hyperacute rejection (b) acute rejection (c) chronic rejection (d) graft-vs-host disease
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