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Path 6 Immuno


epithel barriers block entry of microbes, phagocytic cells (neutrophils and macrophages), dendritic cells, NK cells, and plasma prots (complement sytem). act via inflamm and anti-viral defense (via dendritic and NK cells) Innate Immunity
Mediated by B lymphos and antibods (Igs) protects against extracellular microbes and their toxins Humoral Immunity (adaptive) - IgM and IgD are on the surface and are the antigen binding component of B-cell receptor complex - IgAlpha and IgBeta transduct signals through the antigen receptor
Mediated by T lymphos protects against intracellular microbes Cellular Immunity (adaptive) - AlphaBeta TCR recognizes peptide antigens displayed by MHC on the surface of APCs - CD3 and Zeta prots transduct signals into T cell after TCR has bound antigen
Most important APC for initiating primary T-cell response. located under epithelia (site of entry of microbes/foreign antigens) and in interstitia of all tissues (where antigens may be produced). express TLRs and Mannose receptors. Dendritic cells - Immature = Langerhans cells - Follicular dendritic cells are located in the lymph follicles of the spleen and present antigens to B cells.
phagocytose microbes, process antigens,m present peptide frags to T cells (APCs in T-cell activation). Also, activated/enhanced by T cells to kill ingested microbes. Also, destroy microbes that are opsonized by IgG or C3b Macrophages
endowed w the ability to kill a variety of infected and tumor cells, w/o prior exposure to or activation by them. express CD16 (lyse IgG coated cells) and CD56. Also, secrete IFN-Gamma, which activates macrophages to destroy ingested microbes. NK cells - IL2 and IL15 stimulate proliferation - IL12 activates killing and secretion of IFN-Gamma
Expressed on all nucleated cells and platelets. encoded by HLA-A,B,and C. Consists of Alphas1,2,and 3 and Beta2. Display peptides derived from prots (antigens) located in the CYTOPLASM and usually produced in the cell. Recognized by CD8+ T lymphos Class I MHC molecules
Expressed on cells that present ingested antigens and respond to T-cells (macrophages, B-cells, dendritic cells). encoded by HLA-D. Consists of Alphas1,2 and Betas1,2. Present antigens that are internalized into vesicles and usually from EXTRACELL microbe Class II MHC molecules
Inflamm diseases, including ankylosing spondylitis, are associated w ... HLA-B27
Autoimmune diseases, including autoimmune endocrinopathies, associated w alleles at the ... DR locus - DR3: Chronic active hepatitis, Sjogren synd, Type 1 Diabetes - DR4: Rheumatoid arthritis, Type 1 Diabetes
Th2 and IgE antibods -> mast cell release of histamine -> vasc dilation, edema, smooth muscle contraction, mucus production, inflamm. Ex: Anaphylaxis, allergies, bronchial asthma Immediate (Type I) hypersense
IgG, IgM -> binds to antigen on target cell-> phagocytosis or lysis of target cell. Ex: Autoimmune hemolytic anemia, Goodpasture synd, Myasthenia Gravis, Graves Antibody-mediated (Type II) hypersense
Depot of antigen-antibod complexes -> complement activation -> recruitment of leukocytes by complement -> release of enzymes/toxic molecules. Inflamm, necrotizing vasculitis. Ex: SLE, serum sickness, poststrep glomnephritis Immune complex-mediated (Type III) hypersense
Activated T cells (Th1, Th17, and CTLs)-> release of cytokines (inflamm and macrophage activation) and T cell mediated cytotox. Granuloma formation. Ex: MS, Type 1 Diabetes, RA, IBD (Crohn), TB Cell-mediated (Type IV) - CD4+ = Delayed Type w Th1 -> macrophages and Th17 -> neutrophils (ex poison ivy rxn) - CD4s + IL-12-> Th1 - CD4s + IL-1,6,or 23 + TGF-Beta-> Th17 - CD8+ = Cytotoxicity w perforins and granzymes (ex Type 1 Diabetes)
Gene most frequently implicated in autoimmunity. when dysfunctional -> lack of control of tyrosine kinases -> excess lymphocyte activation PTPN-22
Chronic, remitting/relapsing, often febrile illness w injury to skin, joints, kidney, serosal membranes. black/hispanic young women. malar rash, photosensitive, arthritis, renal probs, seizure/psychosis, hemolytic anemia, ANAs (anti dsDNA/Smith antigen) Systemic Lupus Erythematosus (SLE) - hydralazine, procainamide, penicillamine can induce SLE-like response (antihistone)
nonbacterial verrucous endocarditis w single or multi 1-3mm warty deposits on any heart valve, distinctively on EITHER surface of the leaflets. Libman-Sacks endocarditis
Dry eyes/mouth from immunological destruction of lacrimal and salivary glands. Anti SS-A (Ro) and SS-B (La). 50-60 y/o women. Sjogren synd
Chronic inflamm d/t autoimmunity, widespread damage to small blood vessels, progressive interstitial and perivascular fibrosis in skin and some organs. Diffuse or limited. W limited can have CREST synd. Anti-Scl 70 and anticentromere antibody. Systemic Sclerosis (Scleroderma) - 50-60 y/o black women - CREST = Calcinosis, Raynaud, Esophageal dysmotility, Sclerodactyly, Telangectasia - anti-Scl 70 (against DNA topo I)-> pulm fibrosis and periph vasc disease - anticentromere antibod-> CRE
Kidney rejection w/in mins or hrs after transplant. rapidly becomes cyanotic, mottled, flaccid, and cortex undergoes outright necrosis (d/t infarction) Hyperacute Rejection
Kidney rejection w/in days of transplant in untreated pt or suddenly months-yrs later, after immunosuppression is stopped. - humoral rejection w vasculitis - cellular rejection w interstitial mononuc cell infiltrate Acute Rejection
progressive renal failure w rise in serum creatinine over 4-6 mos. dominated by vasc changes, interstitial fibrosis, tubular atrophy w loss of renal parenchyma Chronic Rejection
Mainstay of immunosuppression. blocks activation of Nuclear Factor of Activated T cells (NFAT), required for transcription of cytokine genes (like IL-2). Cyclosporine
Immuno competent cells transplanted into immuno crippled recipients, and the transplanted cells recognize alloantigens in the host. most commonly w bone marrow transplant. GVH Acute: rash->desquamation, destroy bile ducts->jaundice, mucosal ulcer->dysentery. Chronic: extensive cutaneous injury w destroy skin appendages and fibrosis of dermis, cholestat jaundice, esophageal stricture, involute thymus/deplete lymphos->infx
Failure of B-cell precursors to develop into mature B cells. mutant cytoplasmic Bruton tyrosine kinase (Btk), on long arm of X chromo. males at 6 mos get recurr bac infx of resp tract. B and plasma cells absent, germinal centers underdeveloped, T rxn norm X-Linked (Bruton's) Agammaglobulinemia - Common variable Immunodef affects both sexes equally
European w extremely low serum and secretory IgA, can be familial or acquired w toxoplasmosis, measels, other viral infx. Mucosal defense is weak->resp, GI, GU infx-> recurrent sinopulm infx and diarrhea Isolated IgA Deficiency
Pts make IgM antibods but are deficient in their ability to produce IgG, IgA, and IgE. most are X-linked mutant CD40L (no Ig class switch). Recurrent pyogenic infx and susceptible to Pneumocystis jiroveci Hyper IgM Synd
T cell deficiency d/t failure of 3rd and 4th pharyngeal pouch formation (4th->thymus, parathyroids, ultimobranchial body). Lose T cell-mediated immunity (no thymus), tetany (no parathyroids), and congenital heart/great vessel defects. 22q11 del DiGeorge Synd (Thymic Hypoplasia)
Defects in both humoral and cell-mediated immune responses. Infants w thrush, diaper rash, fail to thrive. Most common form is X linked mut in common Gamma-chain of cytokine receptors. def IL7->lack T cells/impaired antibody synth. def IL15->lack NK cells Severe Combined Immunodeficiency (SCID) - most commoncause of autosomal recessive SCID is def Adenosine Deaminase (ADA)
X-linked recessive w thrombocytopenia, eczema, vulnerable to recurr infx->early death. progressive secondary depletion of T cells in blood and lymphnodes. IgM low, IgG norm, IgA and IgE high. Prone to developing NHL. d/t mutant WASP Wiskott-Aldrich Synd
Most common Complement def -> SLE-like disease C2 (also other early complements like C1s and C4) - def late complements (C5,6,7,8,9) -> no MAC -> susceptibility to recurr Neisseria infx
Most common HIV in US HIV-1 M B
HIV envelope has 2 glycoprots, what are they? and what is the initial step in infx? What are the coreceptors for the recognition site on gp120? Surface gp120 and a transmembrane gp41. Initial step in infx is binding of gp120 envelope glycoprot to CD4 molecules Coreceptors = CCR5 and CXCR4 (homozygous CCR5 defect = AIDS resistance).
Green birefringence with Congo red stain when observed by polarizing microscopy, and Cross Beta-pleated sheet conformation. Amyloid
Systemic disease w AL type prots (from Ig light chains [Bence Jones prots] mainly Lambda, also excreted in urine). Associated w Multiple Myeloma. Primary Amyloidosis
Systemic disease w AA type prots (from SAA). Secondary to inflamm conditions (RA, ankylosing spondylitis, IBD; also Heroin users; and renal cell CA and Hodgkin lymphoma Reactive Systemic Amyloidosis
Deposition of Beta2-microglobulin, w chronic renal fail, can't be filtered -> carpal tunnel synd Hemodialysis-Associated Amyloidosis
Recessive autoinflamm synd w AA type prots and high cytokine IL-1 production. Fever w inflamm of serosal surfaces. Armenians, Sephardics, and Arabics with pyrin gene. Familial Mediterranean Fever
Dominant w deposition of mutant TTR amyloid in periph and autonomic nerves. Familial Amyloidotic Neuropathies
Created by: Jakphooey