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BR-Immunology
5/30/06
| Question | Answer |
|---|---|
| What part of the L and H chain recognizes antigens? | the variable part |
| What part of the H chain of IgM and IgG fixes complement? | the constant part |
| Which chain contributes to Fc and Fab fractions? | the heavy chain |
| Which part contributes only to the Fab fraction? | the light chain |
| Stuff to remember about Fc: (4) | Constant, Carboxy terminal, Complement binding (IgG and IgM only), Carbohydrate side chains |
| What is antibody opsonization? | antibodies promote phagocytosis |
| What is antibody neutralization? | antibody prevents bacterial adherence |
| What is antibody complement activation? | it forms a Membrane Attack Complex (MAC) where antibody activates complement which enhances opsonization and lysis |
| IgG isotype | Most abundant; main antibody in 2* response; fixes complement, crosses PLACENTA, opsonizes bacteria, neutralizes bacterial TOXINS and viruses |
| IgA isotype | Found in Secretions; Prevents attachment of bacteria and viruses to mucous membranes, does not fix complement; Picks up secretory component from epithelial cells before secretion; monomer or dimer |
| IgM isotype | Antigen receptor on surface of B cells; Produced in 1* response to antigen; fixes complement, but does not cross placenta; monomer or pentamer |
| IgE isotype | Lowest [ ] in serum; Mediates Immediate Type I Hypersensitivity by inducing release of mediators from mast cells and basophils when exposed to antigen; Mediates immunity to WORMS |
| Allotype (polymorphism) | Ig epitope that differs among members of SAME SPECIES; can be on heavy or light chain |
| Isotype (IgG, IgA, etc) | Ig epitope common to a single class of Ig (ex: 5 classes all determined by HEAVY chain); iso = same class |
| Idiotype (specific for a given antigen) | Ig epitope determined by antigen-binding site; idio = unique; HYPERVARIABLE region |
| MHC consists of: | 3 Classes if I genes (A, B, C) and 3 Classes of II genes (DP, DQ, DR) |
| All nucleated cells have what type of MHC protein? | MHC I; a single polypeptide with a beta2-microglobin |
| What type of MHC protein is the main determinant of organ rejection? | MHC II; 2 polypeptides with an alpha and beta chain |
| What type of cells have MHC II proteins? | macrophages, dendritic cells |
| Where does MHC I antigen loading occur? | in the RER; they pick up VIRAL antigens |
| Where does MHC II antigen loading occur? | in acidificed endosomes |
| Th 1 cells produce _ and _ which activate _ and _ | IL-2 and interferon-gamma; MQs and cytotoxic T cells |
| Th 2 cells produce _ and _ which help... | IL-4 and IL-5; B cells make antibody |
| Antibody/humoral-mediated immunity | B cells; host defense against infection (opsonize bacteria, neutralize toxins and viruses); Allergies (ex: hay fever); Autoimmunity |
| Cell-mediated immunity | T cells; host defense against infx (esp M. tuberculosis, virus-infected cells and fungi); Allergies (ex: poison oak); Graft and tumor rejection; Regulation of antibody response (help and suppression) |
| Adjuvants (ex: vaccines containing aluminum hydroxide or lipids) | nonspecific stimulators of the immune response; not immunogenic alone; these are given with a weak immunogen to enhance response |
| Helper T cells have CD4, which binds to... | MHC II on APCs |
| Cytotoxic T cells have CD8, which binds to... | MHC I on any virus-infected cell in the body |
| CD3 Complexes | clusters of polypeptides a/w a T cell receptor; they are important for signal transduction |
| Which cells are Antigen Presenting Cells? | MQs, Bcells, Dendritic cells |
| Activation of T helper cells (4 steps) | 1. foreign body phagocytosed by APC; 2. Foreign antigen presented on MHC II and recognized by TCR on Th cell; 3. "Co-stimulatory signal" is given by interaction btw B7 & CD28; 4. Activated Th cell produces IL-2 and IFN-gamma |
| IL-2 specifically activates... | cytotoxic cells (CD8) |
| Interferon-gamma (from helper T cells) specifically activates | macrophages |
| What activates a naive (Th0) cell to differentiate? | IL-12 (from MQ) and IL-4 (from some human cell); IL-12 induces Th1 (CD8 path) and IL-4 induces Th2 (B-cell path) |
| Cytotoxic Tcell activation occurs when... | endogenously synthesized (viral or self) proteins are presented on MHC I and recognized by TCR on Tc cel; IL-2 from Th cell activates Tc to kill virus infected cell |
| What is Anergy? | A state of non-responsiveness to aT or B cell's specific antigen, even in optimal conditions of stimulation |
| How can I remember important cytokines? | "Hot T-bone stEAk" |
| what does "Hot T-bone stEAk" stand for? | IL-1 (hot; fever); IL-2 (T cells); IL-3 (bone marrow); IL-4 (IgE); IL-5 (IgA) |
| IL-8 function | chemotactic for NEUTROPHILS |
| TNF-alpha | secreted by MQs; increases IL-2 receptor synthesis by helper T cells; Increases B cell production; Attracts and activates PMNs |
| TNF-beta | secreted by activated T lymphos; similar function to TNF-alpha (inc IL-2 synth, inc Bcell proliferation, attracts/activates PMNs) |
| What kind of markers are on a T helper cell? | CD4, TCR, CD3, CD28 |
| What kind of markers are on a Cytotoxic T cell? | CD8, TCR, CD3 |
| What kind of markers are on a B cell? | IgM, B7, CD19, CD20 |
| Which markers are on MQs? | MHC II; CD14 |
| Which markers are on NK cells? | receptors for MHC I, CD16 |
| What is the only cell type in the body that doesn't express MHC I? | mature RBCs |
| Which cytokines are responsible for initiating the Acute Phase Response? | IL-1, IL-6, and TNF-alpha |
| What is activated in an Acute Phase Response? | Bcells (Abs), Tcells (cytotoxicity), PMNs (phagocytosis), Liver (acute phase reactants/compl/opsoniz), BM (colony stim/leukocytosis); Hypothalamus (inc temp); Fat/muscle (energy/temp); APCs (TNF-a for migration to nodes/adaptive response) |
| Increased body temperature does what in an Acute Phase Response? | increases specific immune response, increases antigen processing, decreases viral and bacterial replication |
| Complement defends against what type of pathogen? | Gram-negative bacteria |
| What activates complement 's CLASSIC Pathway? | IgG or IgM; "GM makes Classic cars" |
| What activates complement's ALTERNATE Pathway? | molecules on the surface of microbes (especially ENDOTOXIN) |
| Complement Function: C1, C2, C3, C4 | Viral neutralization |
| Complement Function: C3b | Opsonization |
| Complement Function: C3a, C5a | Anaphylaxis |
| Complement Function: C5a | Neutrophil chemotaxis |
| Complement Function: C5b-C9 | Cytolysis by MAC (membrane attack complex) |
| Deficiency of C1 esterase inhibitor leads to: | Hereditary Angioedema d/t overactive complement |
| Deficiency of C3 leads to: | Severe, recurrent pyogenic sinus and respiratory infections |
| Deficiency of C6-C8 leads to: | Neisseria bacteremia |
| Deficiency of Decay-Accelerating Factor (DAF) leads to: | Paroxysmal Nocturnal Hemoblobinuria (PNH) |
| Inferferons (alpha, beta, gamma) are proteins that... | Interferes with viral protein synthesis (put uninfected cells in an antiviral state; they induce the production of a 2nd protein that inhibits viral protein synthesis by degrading its mRNA) |
| alpha and beta interferons | inhibit viral ptn synthesis |
| gamma-interferon increases expression of: | MHC I and II and antigen presentation in all cells AND activates NKs to kill virus infected cells |
| Type I hypersensitivity | anaphylactic and atopic; Ag x-links IgE on presensitized mast cells & basophils triggering release of vasoactive amines; rapid rxn d/t preformed Ab; ex: anaphylaxis, asthma, hives, local wheal and flare |
| Type II hypersensitivity | Cytotoxic; IgM & IgG bind Ag on "enemy" cells, cause lysis (by complement) or phagocytosis; Ex: Autoimmune hemolytic anemia, Rh dz, Goodpasture', Rheumatic fever, Graves dz, bullous pemphigoid); Ab + Complement = MAC (membrane attack complexes) |
| Type III hypersensitivity | Immune Complex (Ag-Ab-Complement), Serum Sickness (5 days post drug exposure, immune complexes are deposited in membranes, fix complement & causing tissue damage), or Arthus reaction (intradermal local edema, necrosis, complement activation) |
| What are some symptoms of serum sickness (type III hypersensitivity)? | fever, urticaria, arthralgias, proteinuria, lymphadenopathy; all developing 5-10 days after antigen exposure |
| Type IV hypersensitivity | delayed (cell-mediated) type; sensitized T cells encounter Ag and then release lymphokines leading to MQ activation; Ex: Transplants, TB tests, Touching (contact dermatitis) |
| Bruton's Agammaglobulinemia (B cell deficiency) | XR (Boys); Low levels of all Ig classes; Recurrent Bacterial infxns after 6mo when mom's IgG declines; defective Tyrosine Kinase (BTK) |
| Selective Immunoglobulin deficiency (B cell deficiency) | Selective IgA is most common; Sinus & Lung infections; Deficiency in a specific Ig class (possibly d/t defect in isotype switching); |
| Thymic Aplasia/DiGeorge Syndrome (T cell deficiency) | Failure of 3rd/4th pharyngeal pouches; Presents as Tetany (hypocalcemia); Recurrent viral/fungal infxns; CATCH 22 (cardiac, abnml facies, thymic hypoplasia, cleft palate, hypocalcemia, 22-chrom); |
| Chronic Mucocutaneous Candidiasis | T cell deficiency specifically against Candida albicans; Presents with skin/mucous infxns |
| Severe Combined Immunideficiency (SCID) | Defect in early stem cell differentiation (No B or T cells); Recurrent Viral, Bacterial, Fungal, & Protozoal infxns; may have multiple causes (failure to synthesize MHC II antigens, defective IL-2 receptors, Adenosine deaminase deficiency) |
| Wiskott-Aldrich Syndrome (T and B cell deficiency) | X-linked defect in ability for IgM response to CAPSULAR polysaccharides of bacteria; Elevated IgA, Normal IgE, LOW IgM; Recurrent pyogenic infxns, thrombocytopenic Purpura, Eczema |
| Ataxia-Telangiectasia (B and T cell deficiency) | Defective DNA repair enzymes & IgA deficiency; Cerebellar/ataxic (18mo) problems and Spider Angiomas (school age) |
| Chronic Granulomatous Disease | defect in PMN phagocytosis d/t lack of NADPH oxidase; Susceptible to OPPORTUNISTIC infxns (S. aureus, E. coli, Aspergillus, Salmonella, Nocardia); Dx Confirmed with Negative Nitroblue Tetrazolium dye reduction test |
| Chediak-Higashi Disease | Auto Recessive; vesicle fusion defect/microtubular fxn/lysosomal emptying of phagocytic cells; Recurrent Pyogenic infxns by Staph and Strep; Granulomas affecting many organs |
| Job's Syndrome | Recurrent "cold" (non-inflamed) staph abscesses, eczema, High IgE; Failure of gamma-interferon production by Th cells; PMNs fail to respond to chemotactic stimuli |
| Leukocyte Adhesion Deficiency Syndrome | Defect in LFA-1 adhesion proteins on Phagocytes; Early life, severe Pyogenic infxns and wound healing problems |
| Hyper-IgM Syndrome | Defect in CD40 Ligand on CD4 Thelper cells leads to inability to class switch; Presents early in life w/Severe Pyogenic infxns; Very High IgM (very low IgE, IgG, IgA); Sores in mouth d/t granulocyte deficiency |
| IL-12 Receptor Deficiency | Presents with Disseminated Mycobacterial Infections (IL-12 needed for activation of Th0 to transform into Th1 cells for MQ/CD8 activation; DO NOT Give BCG vaccine |
| Active Immunity | induced after exposure to foreign Ag; slow onset; long-lasting protection (memory) |
| Passive Immunity | pt's are given preformed Abs "To Be Healed Rapidly" = Tetanus toxin, Botulinum toxin, HBV, or Rabies; Rapid onset; Short lifespan of Abs in pt |
| Antigen variation: Bacteria | Salmonella (2 flagellar variants); Borrelia (relapsing fever); Neisseria gonorrheae (pilus protein) |
| Antigen variation: Virus | Influenza (major = shift (RNA segment rearrangemen); minor = drift) |
| Antigen variation: Parasites | Trypanosomes (programmed rearrangement) |
| Hyperacute Transplant Rejection | Ab-mediated d/t presence of PREFORMED anti-donor antibodies in recipient; occurs w/in MINUTES; Type I hypersensitivity |
| Acute Transplant Rejection | Cell-mediated d/t cytotoxic Tcells reacting against foreign MHCs; occurs weeks after transplantation; reversible with immunosuppressants such as cyclosporin or OKT3; Type IV hypersensitivity |
| Chronic Transplant Rejection | Antibody mediated vascular damage; Fibrionoid necrosis; Occurs months to years after transplantation; IRREVERSIBLE |
| Graft-versus-host disease | Grafted immunocompetent T cells proliferate in irradiated immunocompromised host and reject cells with "foreign" proteins, resulting in SEVERE HOST ORGAN FAILURE; Maculopapular rash, Jaundice, Hepatosplenomegaly, Diarrhea |
Created by:
bscaryp