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| 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
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| 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
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| 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
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| 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.
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| 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
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| 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
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| 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
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| 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
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| Inflamm diseases, including ankylosing spondylitis, are associated w ... | HLA-B27
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| 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
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| 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
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| 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
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| 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
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| 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)
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| Gene most frequently implicated in autoimmunity. when dysfunctional -> lack of control of tyrosine kinases -> excess lymphocyte activation | PTPN-22
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| 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)
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| 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
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| 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
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| 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
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| Kidney rejection w/in mins or hrs after transplant. rapidly becomes cyanotic, mottled, flaccid, and cortex undergoes outright necrosis (d/t infarction) | Hyperacute Rejection
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| 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
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| 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
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| Mainstay of immunosuppression. blocks activation of Nuclear Factor of Activated T cells (NFAT), required for transcription of cytokine genes (like IL-2). | Cyclosporine
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| 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
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| 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
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| 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
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| 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
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| 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)
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| 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)
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| 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
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| 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
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| Most common HIV in US | HIV-1 M B
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| 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).
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| Green birefringence with Congo red stain when observed by polarizing microscopy, and Cross Beta-pleated sheet conformation. | Amyloid
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| 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
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| 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
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| Deposition of Beta2-microglobulin, w chronic renal fail, can't be filtered -> carpal tunnel synd | Hemodialysis-Associated Amyloidosis
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| 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
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| Dominant w deposition of mutant TTR amyloid in periph and autonomic nerves. | Familial Amyloidotic Neuropathies
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