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71 Cards in this Set
- Front
- Back
Innate immunity
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That state of immunity with which one is born. It exists regardless of exposure to antigen and is not enhanced by repeated exposure to antigen.
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Adaptive immunity
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State of immunity that is developed as a result of
exposure to an antigen. It is specific for the particular antigen and is enhanced following repeated exposure to the same antigen. |
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CD
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Cluster of Differentiation – a nomenclature system that classifies many molecules on
immune and hematopoietic cells. Numbers next to the CD only denote the order in which the molecule was discovered. CD3, CD4 and CD8 are markers for T cells, CD19 & 20 for B cells. |
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Passive--Generally and Natural immunity
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Passive Immunity (generally): Normally occurs when specific (pre-formed) antibody or serum) is
transferred from an immunized individual to a non-immunized individual. Antibodies or sera are usually obtained from humans or animals that have been deliberately immunized or have naturally recovered from active infection. Natural - protective antibody (IgG) transferred from mother to infant via placenta (e.g. against diphtheria, tetanus, mumps, rubella), responsible for immunity in the first few months to 1 year of life |
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Passive - artificial immunity
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Artificial –necessary in:
i. individuals who cannot make antibodies (SCID patients) ii. immunocompromised individuals who might develop disease before active immunization can stimulate a protective immune responses (usually in 7-10 days). Examples include cancer patients undergoing radiation and chemotherapy and human immunoglobulin against Hepatitis B or cytomegalovirus (CMV) iii. individuals exposed to deadly toxins (e.g. from snake or black widow spider bite; tetanus toxin). |
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Passive - adoptive immunity
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A form of passive immunization that involves the transfer of
cells with the ability to confer immunity. Usually involves transfer to the same (autologous) host (e.g. adoptive transfer of T cells in cancer immunotherapy). |
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Commensal flora
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one of the essential functions of these commensal microorganisms is to
participate in protecting skin and mucosae from invasion with microbial pathogens. Commensals compete with pathogenic microorganisms for nutrients and also present a physical barrier to invasion. |
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Facultative pathogens
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Sometimes, normal flora on the skin or in the gut can become pathogenic due to special
circumstances, for example when the fungus Tinea cruris/pedis, which normally lives on the skin becomes pathogenic because the integrity of the epidermis has been mechanically or otherwise compromised (jock itch or athlete’s foot). |
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Obligatory pathogens
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microorganisms that cause diseases can be classified
into three main homogenous families, bacteria, viruses and fungi, and the fourth, heterogenous group, parasites, which include pathogens such as intracellular protozoa (e.g. Plasmodium malarie, Trypanosoma brucei) and large multicellular, chiefly intestinal, worms (e.g. schistosoma, tapeworms). |
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Hematopoietic stem cells
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bone marrow derived
precursor to all cellular elements |
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Common myeloid progenitor
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1) common granulocyte precursor
2) Unknown precursor that leads to a) monocyte --> dendritic cell, macrophage, mast cell |
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Common lymphoid progenitor
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1) B cell
2) T/NK cell precursor --> T cell, NK cell |
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Common granulocyte precursor
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Neutrophils, basophils, eosinophils
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Common erythroid megakaryocyte progenitor
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1) megakaryocyte --> platelets
2) erthyroblast --> erythrocyte |
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primary lymphoid organ
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site of lymphocyte
development, i.e. where lymphoid stem cells proliferate and differentiate into mature cells (lymphopoiesis). Location where lymphocytes acquire antigen receptors and learn to distinguish “self” from “non-self”. |
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Innate immunity vs. adaptive immunity
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Innate:
- Exists prior to exposure to antigen - response not enhanced by repeated exposure - no antigen specific response - no immunological memory - several physical components (see other flashcard) - biochemical components (complement, lysozyme, low pH, interferons) - neutrophils, monocytes, NK cells, macrophages, DC, NKT cells Adaptive - Developed in response to antigenic insult/encounter - resistance improved by repeated exposure - immunologic memory - no physical components - biochemical components include: antibody and lymphokines (IL2, IL4, IFN-gamma, IL5) - Cells: B and T lymphocytes, DC |
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Physical components of innate immunity
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skin, mucus, coughing, sneezing, crying; urination, competition for space and nutrients by host normal
flora; epithelial tissues produce antimicrobial peptides (e.g., defensins) |
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Sequence of inflammatory events (general)
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1) Vasodilation
2) Increased vascular permeability 3) Influx of immune cells 4) Elimination of pathogen, tissue repair and regeneration |
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Sequence of inflammatory events (in depth)
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1) The infectious pathogen at the site sends a “danger signal” to tissue macrophages and dendritic cells when it binds to cell Toll-like receptors (TLR)
2) cause recruitment of leukocytes, activation of anti-microbial activity & get the adaptive immune responses going 3) The macrophages are stimulated to secrete inflammatory cytokines (IL-1 and (TNF-α) that increase expression of adhesion molecules on endothelial cell surfaces --> recruit immune cells from blood. Also, chemokines {IL-8, macrophage chemotactic protein-1 (MCP-1), RANTES} 4) immune cells ingest/degrade the pathogens. 5) Immature dendritic cells (as well as macrophages) at the infection site also pick up a pathogen and its antigens and are induced to mature by the “danger signal”. 6) Matured DCs (and macrophages) then migrate via the lymphatic system to the lymph node draining the infection. 7) The DC “present” the pathogen’s antigens to T cells and stim division and differentiation into pathogen-specific effector lymphocytes. |
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TLR characteristics
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TLRs are a bridge
between innate and adaptive immune systems, causing recruitment of leukocytes, activation of anti-microbial activity & get the adaptive immune responses going. TLR are invariant, hardwired, and often more than 1 per cell is expressed. Some are extracellular where they bind bacteria and their byproducts, while others are intracellular where they bind to viruses and their products. Different combinations of TLRs produce a combinatorial recognition repertoire which recognizes invariant microbial molecules. There are 10 TLRs identified in humans; TLR4 recognizes Gram-negative bacteria while TLR3 recognizes viral RNA. |
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Immunogen
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An antigen that is capable of binding to components of the immune response and evoking an immune response such as the production of antibodies or secretion of cytokines.
all immunogens are antigens but not all antigens are immunogens |
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Hapten
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molecule that is capable of binding to an antibody but unlike an immunogen, is
unable to evoke an immune response such as antibody production. Can bind only to a single antigen binding site (paratope) on an antibody molecule.(antibody molecule has two antigen binding sites). Ex) low molecular weight compounds (dinitrophenol {DNP}, benzene), drugs (aspirin) and antibiotics (penicillin). Can be immunogenic when conjugated to carriers. Ex) Hib vaccine. influenzae polysaccharide covalently linked to tetanus toxin. Abs ar emade against both parts, even though only the carrier is recognized by T cells. |
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Epitope
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(antigenic determinant): Portion of antigen that combines with antibody or T cell receptor. An immunogen generally contains numerous epitopes
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Kinetics of antibody production (phases)
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Lag phase - time btwn initial exposure and detection of Abs (4-7 days in primary response)
Exponential phase: rapid inc in circulating Abs due to inc # and activity of Ab-secreting plasma cells Steady state - Ab synth = degradation Declining phase - antibody synth wanes as immunogen is eliminated |
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Primary vs. Secondary immune response
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Secondary responses have shorter lag time, extended plateau and slower AB decline. Affinity of Abs is higher in secondary as well.
Primary - IgM. Secondary - IgG |
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BCR/Antibody structure
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Bound antibody (with transmembrane anchor domain) is called B cell receptor (BCR)
- 2 heavy chains (one variable VH and 3 constant domains - CH1, CH2, CH3) - 2 light chains (one variable VL and one constant domain CL) - CH1 and CH2 on heavy chain are linked via a flexible linker - hinge region that allows pivoting and optimal Ag binding |
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TCR structure
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Always membrane bound and can only recognize its antigen when bound to the self MHC molecule
- 1 variable domain and one constant domain - W/n Variable domain there is a framework region (FR) and loops of complementarity-determining region (CDR). The CDRs contact pMHC complex and recognize antigen. - CDR1 and CDR@ are less variable and interact mostly with MHC - CDR3 dominantly interacts with peptide Ag in MHC groove TCR interactions with peptide:MHC complex are always weak, which helps T-cell discriminate between self and foreign peptides bound to MHC |
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Antigen binding - Affinity vs. Avidity
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Affinity - strength of bond between a single epitope and a single antigen binding site on the receptor. depends on H bonds, electrostatic fores, hydrophobic forces, and van Der Waals.
Avidity - strength of the multiple interactions btwn a multivalent antigen and a bivalent/multivalent receptor. ex) sum of all interactions between all available TCR molecules and all MHC molecules bearing the antigenic peptide. Avidity predominates bc most natural antigens have multiple epitopes; high avidity can supercede low affinity (IgM vs. IgG) Affinity and avidity determine whether a given lymphocyte will be activated (threshold for activation) |
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Cross-reactivity (examples)
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Ability of a receptor to react with antigen other than the one which originally activated it.
Examples: 1) Abs against cowpox cross react with epitopes of variola virus (smallpox) 2) Antibodies against S. pyogenes M protein cross-react with heart tissue --> rheumatic fever 3) Abs against inactivated tetatnus toxin are protective against the tetanus toxin |
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7 Factors of immunogenicity
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1) Foreignness, phylogenetic distance (except highly conserved molecules)
2) replicability (live vacs are more immunogenic than live attenuated/dead). inc copy number 3) HIgh molecular weight >6000 daltons 4) chemical complexity 5) degradability (must be degraded and processed by APCS to be immunogenic) 6) Responding organism's genetics - absence of MHC molecules/TCR/BCR = lack of response 7) dose of immunogen/route of admin. SubQ is better than IP or IV (diffuse more slowly more likelihood of interact with dendritic cells and langerhans cells. Too low or too high a dose can lead to failure to induce immune response or to tolerance. |
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CD4 T cells
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Also known as Th cells. express CD4, secrete numerous cytokines, help activate dendritic cells?, help B lymphocytes to produce antibodies, help CD8 T cells to mature and produce cytokines
- can also directly eliminate microbial pathogens - or induce macrophages to kill pathogens CD4 T cells can also be further divided into Th1, Th2, and Th17 depending on what tyupe of cytokines they make |
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CD8 T cells
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also called cytotoxic cells.
destroy microbe-infected cells and tumor cells by direct killing - stop microbial invasion by secreting cytokines |
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T reg cells
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express CD4
regulate immune responses by controlling the activities of other immune cells (including other T cells) |
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Cytokines of
Th1 Th2 Th17 T-reg |
Th1 - IFN-1, IL-12, IFN-gamma
Th2 - IL-10, IL-4, IL-5, IL-13, IL9 Th17 - IL-6 + TGFb + IL-22 Treg - IL-6 + TGFb |
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MHC class I structure
function |
all nucleated mammalian cells express class I
- heterodimer of an alpha chain non-covalently boun to B2-microglobulin (B2m) - alpha chain has three domain, 1, 2, 3. - a1 and a2 form the peptide-binding cleft Class I survey the intracellular environment and thus are key in defending against viruses, ic bacteria, parasites, and tumors |
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MHC class II structure
function |
only APCs and thymic epithelial cells normally express class II
- 2 non-covalently bound chains, alpha and beta - alpha chain has a1 and a2 domains - beta chain has b1 and b2 domains - peptide binding cleft is made from a1 and b1 class II molecules dominantly survey ec compartment, response against extracellular microbes |
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Generation of MHC class I binding peptides
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- Pathogen proteins are degraded into peptides in the cytosol by proteasomes
- peptides are transported to the ER by transporter associated with antigen processing-1 and -2 (TAP1 and TAP2) - peptides are trimmed and loaded onto MHC1 in the ER, trans via golgi to the cell membrane CD8 cells |
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Generation of MHC class II binding peptides
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Th1 and Th2 cells
-extracellular pathogens in the ecf taken up by phagocytosis - degraded in phagolysosome - newly synth MHCII molecules in the ER are prevented from binding peptides in the ER bc they are associated with invariant chain (IC). IC is degraded in the endocytic vesicle |
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Type I hypersensitivity
Pathogenesis Examples Clinical diagnosis |
Basics: IgE antibodies binding to mast cells, immediate. anaphylactic shock
Atopic ppl are genetically predisposed to make IgE in response to certain antigens (instead of IgG). and to have higher levels of eosinophils. Primary exposure - sensitization via Th2 stimulating B cells to make antigen-specific IgE. IgE )made after class switching) binds to mast cells (or basophils) via FCe receptors. Secondary: effector phase. Antigen binds to IgE on mast cells. cross-linking of IgE causes granule and cytokine release. (See other flashcards) Ex) allergic rhinitis, allergic asthma, hives, eczema, anaphylaxis Clinical - do an intradermal injection of allergen and see wheal and flare reaction (edema and erythema). takes 10-15 mins. see late reaction in 5-8 hrs. Do RAST test (see other card) Treatment see other card |
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Treatment of Type I hypersensitivity
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1) Avoid allergan
2) Allergen-specific immunotherapy - give very low dose allergen over months, grad. inc. to induce blocking IgG antibodies. (IgG Abs would suck up all the allergen before it gets to IgE on mast cells). 20-30 shots. 3) Desensitization - low doses every 15 mins to slowly trigger all mast cells - penicillin in ICU. 4) Mast cell stabilization - drugs that block degranulation - sodium comoglycate 5) mediatior antagonists - antihistamines, epi 6) Steroids (block PGs) 7) Anti-IgE monoclonal Abs. Omalizumab (IgG1 subclass) binds Fc portion of IgE to block IgE from binding to FCe receptor on mast/basophil. Works great, but pricey. |
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RAST test
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radioallergosorbent test
1) Bind antigen to cellulose disc 2) Put pts. serum IgE on it. 3) Wash away excess 4) Put a radiolabeled anti-IgE antibody in it. 5) Wash away excess. The amt of radiolabeled Ab = amt of IgE in pts. serum |
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Mediators of Type I hypersensitivity
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1) Histamine - smooth muscle contraction. inc vasc permeability (edema)
2) ECF-A (eo chemotactic factor) - attracts eos 3) Leukotrienes C4 and D4 - prolonged smooth muscle contraction and inc. vasc. permeability 4) PAF (platelet activating factor) - causes platelets to release histamine --> bronchoconstriction, vasodilation, local THROMBOSIS 5) Thromboxanes/PGs - vasoactive, bronchoconstriction, LEUKO chemotactics 6) IL-3, 4, 5 (most important), GM-CSF, TNF-alpha: IL- 5 stimulates bone marrow to make more eos! ILs increase adhesion molecules on endothelium. |
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Type II hypersensitivity
Pathogenesis Examples |
Basics - Antibody dependent cellular cytotoxicity. Antigen on cell surface.
1) Foreign antigen on cells induces Ab formation. 2) Ab binds to cells --> act. complement ("fixes") and induces lysis and phagocytosis. 3) Ab can also bind to Fc receptor to any cell that has an FcR and induce ADCC. like NK. Ex) 1) Transfusion reactions. 2) Erthyroblastosis fetalis - anti-Rh antibodies in mom (made from previous kid exposure) cross placenta and destroy fetus RBCs. 3) Autoimmune hemolytic anemia 4) Goodpasture's. Ab binding on basement membrane (see smooth deposits). Pulm hemorrhage/glomerulonephritis 5) Rheumatic fever. Ab to Step M protein damages heart/kidney via cross-reactivity 6) Drug-induced rxn 7) Anti-receptor disease: myasthenia, grave's 8) Graft rejection - preformed Abs to HLA antigen causes severe nonreversible damage to graft. Clinical: check presence of Abs against antigen via ELIZA or Western. OR biopsy. Decreased renal function, pulm infilitrates, hemoptysis, low platelets Treat: prevention by blood cross-matching. Rhogam for Rh- mother with Rh+ babies, supportive plasmapheresis/dialysis, immune suppressants. |
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Type III hypersensitivity
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1) Abs combine with free Ag to make insoluble complexes, which deposit on blood vessel walls.
2) Complexes act. complement. chemoattractant (C5a > C3a) and anaphylatoxin (C3< C4< C5) 3) PMNS (neutros) release lysosomal enzymes and damage the vessel/tissue 3 Types 1) Persistent infection, usually IC --> kidney/infected organ 2) AI - kidney, joint, arteries, skin 3) extrinsic/env antigen --> lung Biopsy - humpy-bumpy immune complex deposits in SLE patients (renal sections) |
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Examples of Type III hypersensitivity
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1) serum sickness - AB response to passive immunization w/ foreign antiserum
2) RA - rheumatoid factor is IgM against Fc part of IgG that deposits in joints. 3) Infectious disease - malaria, viral, fungal, leprosy 4) Farmer's lung (moldy hay spores) 5) Arthus - 6) Glomerulonephritis (post-strep. has to be humpy bumpy biopsy) 7) SLE - AB against DNA. Treat - supportive care. Immunosuppressants |
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Three types of IV hypersensitivity
overview of mechanism |
1) Contact
2) Tuberculin 3) Granulomatous Sensitization then activation. 1-2 weeks after Ag exposure to generate Th1 cells? 1) Th1 cells (sometimes Th17) enter tissue where an APC presents an antigen on MHC II. 2)Th1 cells secrete cytokines (IL2, IFN-gamma, TNFalpha, IL17), chemokines, cytotoxins that make MACROS come/be activated 3) Activated macrophages kill things and destroy tissue |
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Contact hypersensitivity
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Max response 2-3 days
- eczema at site of Ag (as opposed to type I hypersensitivity) - EPIDERMAL Most common causes: heavy metals (nickel, chromate), rubber, poison ivy/oak. Latex. Test by patch test. Heavy metals haptenate cell surface proteins and induce DTH via binding to TLR4, mast cells involved |
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Tuberculin hypersensitivity
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- 2-3 days max rxn
- DERMAL - mostly macros involved |
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Granulomatous hypersensitivity
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Takes at least 2 weeks but up to months to develop.
All the other stuff happens. Also, plasma cells and Cytotoxic T cells come to site may cause tissue damage as well. but then Macrophages can't kill agent/intracellular organism. So, forms epitheloid cell. then fibrosis to wall off the thing. Prominent in parasitic infections (eggs), Fungus, sarcoidosis, and Crohns. filamentous bacteria. |
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Anaphylaxis respiratory components
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1) Bronchial constriction
2) Increased mucus production 3) Larygeal edema causing obstruction(!!) 4) Air trapping (blebs) bc expiration is a passive process also have urticaria Shock and death w/n minutes |
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Tissue changes in local Type I hypersensitivity
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Localized swelling and redness
anaphylaxis is systemic |
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mast cell mediators
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1) Histamine
2) Neutrophil chemotactic factor 3) Enzymes 4) Proteoglycans 5) leukotrienes 6) Pgs 7) Cytokines (TNF, IL-1) HELPP-PCT |
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Late phase reaction
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more destructive
Major role in eosinophils Release of proteolytic enzymes, major basic protein, and eosinophilic cationic protein Cause epithelial damage/lysis, stimulate further mast cell granule release recruitment of additional leukocytes |
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Mechanism of allergen-specific immunotherapy
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Periodic injections of allergen with increasing dose
Shifts response from IgE to IgG blocking antibodies which do not react with mast cell receptors |
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Three mechanisms of hypersensivity
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1) Antibody mediated cell destruction via complement (major)
2) Cell/tissue destruction by NK lymphocutes 3) Antibody binding altering function (myasthenia, graves) |
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Transfusion reaction mechanism
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Result of ABO or Rh incompatability btn donor and recipient.
Circulating Abs against the donor's blood initiate lysis of RBCs. hbg released in plasma --> cardiovascular collapse --> shock/death |
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Hemolytic disease of the newborn
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Rh+ father, Rh- mother
1) In the first pregnancy the fetus's Rh+ blood evokes an immune response from mom of the IgM type which cannot cross the placenta. 2) In the second pregnancy, the mom produces IgG which can cross the placental barrier. 3) The fetus's RBCs are destroyed in utero. Use Rhogam |
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Pemphigus vulgaris vs. Bullous pephigoid
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PV vs. BP = desmosomes vs. hemidesomosomes
PV - Ab against desmoglein 1 and 3 which destroyes intercellular attachments in epidermis. - causes separation of upper levels of epidermis from the basal layer BP - Antibody against BPAG1 (a plakin) and BPAG 2 (collagen type 18) destroys hemidesmosomes - Complete epidermal separation from dermis - 10-15% also have mucosal involvement. Can test by direct Immunofluoresence of lesional skin. Or indirectly. |
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Type III hypersensitivity facts
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- small and medium sized complexes (large get phaocytosed by macrophages)
- injury occurs in those places that filter blood (glomerulus, synovium, choroid plexus in brain, dermal capillaries of skin) - Don't forget that platelet aggregation may lead to microthrombi and ischemic tissue damage - levels of complement will fall when complexes activate it --> measure to diagnose - Immune complexes containing IgG and IgM antibodies (which fix complement) and Abs which bind to white blood cell Fc receptors are most pathogenic - Endothelial cells play a role through production of IL 1,6,8, and CAM, proteolytic enzymes |
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Post-infectious Glomerulonephritis (Streptococcus)
Symptoms, tests "humpy bumpy pig" |
Can be caused after both pharyngitis AND skin infections by Group A beta-hemolytic Strep
Takes at least 7-10 days after infection (up to 2-4 weeks) Symptoms - actue salt and water retention --> edema and HTN May need dialysis and other supportive care. Kids do great. Adults may have chronic issues like hemat/proteinuria Histo - will see endothelial and mesangial proliferation. Lots of neutrophils and monocytes --> nothing is getting filtered in the kidney Fluoresence will show lumpy bumpy fluoresence in glomerulus |
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Causes of Type III hypersensitivity
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1) Infectious - strep, hepatitis, syphilis, malaria
2) Neoplastic - breast ca, melanoma, lung ca 3) Serum sickness - IgG from animal is the antigen for the body |
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Components of granulomas
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Tb and cocci among others (add!)
Monocytes differentiate into macrophages AND epithelioid cells Outer edge - fibroblasts, "guarding" memory T cells, macros Center - epithelioid cells, giant cells. NO neutrophils - actually inhibited by a factor. Macrophages are inhibited from leaving. |
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Hyperacute rejection of transplanted organs
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hallmark is pre-formed antibodies
within minutes ex) kidney turns black on the operating table when blood flow is re-established |
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Acute cellular/acute humoral rejection
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variable time course, first months after transplant.
Target is usually tubules and blood vessels. Cellular rejection more common (CD4+ and CD*+ T cells) Humoral targets the endothelium more. |
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Chronic transplant organ rejection
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Progressive vascular narrowing and tissue ischemia due to multiple episodes of rejection
usually over years |
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Cell markers for Hematopoietic stem cells
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CD34 and/or CD133+
no CD3, CD19, etc. HSCs are self-renewing cells located in bone marrow but a few also circulate in blood |
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Cell markers for B2 cells vs. B1 cells
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B2 - CD19
B1 - CD 5 (i think check!) |
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B cell development
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- Occurs in bone marrow
- dependent on exp of ADHESION molecules - dependent on STROMAL secretion of CYTOKINES and GROWTH FACTORS - develop in islands of hemtapoietic development - niches 1) A stem cell/lymphoid progenitor docks onto a BM stromal cell with VLA-4 binding to VCAM-1 FINISH THIS |
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Clinical consequences of lack of/removal of lymphoid organs
- Bone marrow - spleen - thymus - lymph node |
1. Bone marrow – damage - aplastic anemia; SCID defect, etc
2. Thymus – congenital – T cell deficiency; removal - early attrition and aging of T cells 3. Spleen – polycythemia; defective Ab responses, susceptibility to encapsulated bacteria 4. LN – rarely indispensible, lymphoedema |
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Innate immunity activation (steps)
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1) TLR and NLRs on DC and macrophages get a "danger signal" when they bind to infectious pathogens
2) Macros are stimulated to secrete inflam cytokines like IL-1 and TNFalpha that inc expression of adhesion molecules on endothelial cell surfaces. Also secrete chemokines (IL8 and macro chemotactic protein, rantes) 3) The inc expression of adhesion molecules causes more immune cells from blood to go to inflammatory site. 4) Complement components (C3a, C5a) with chemotactic activity are also produced at te site. 5) Now that neutros and monocytes are at site they ingest and degrade the pathogens. 6) immature DCs at the site pick up pathogen and are induced to mature by the danger signal. They migrate via lumphatic system to lymph node to present the pathogen's antigens to T cells. |
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Leukocyte Adhesion Deficiency
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A deficiency in expression of LFA-1 and Mac-1, leading to impaired recuitment of blood cells to the site of inflammation.
Mutation in the gene encoding the Beta2 subunit (CD18) of the integrin proteins LFA-1 and Mac-1. They are heterodimeric. LFA-1 is CD11a:CD18 (binds to ICAM-1,2) Mac-1 is CD11b:CD18 (binds to the same) Prone to recurrent bacterial infections and impaired wound healing. |