Created by Jessica Margaux Mercado
about 9 years ago
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Question | Answer |
NKT cell surface receptor | CD8 |
Suppressor T-cells (pan T-markers, receptor/s) | CD2 CD3 CD5 CD8 |
Helper T-cell (receptor/s) | TCR CD4 |
TH1 (antibody, action, secretion) | IgG opsonization, complement fixing IL-2, IFN-gamma |
TH2 (antibody, action, secretion) | IgE activate eosinophil IL-4, IL-5, IL-13 |
B-cell receptor (for maturation and secretion of Ig) | CD40 |
NK cell (surface markers, receptor/s) | CD16 CD56 CD8 |
pan B marker | CD19 |
indicates B lymphoid lineage (marker) | Surface Ig Cellular Ig |
pan T-cell Ab | CD2 CD3 CD5 CD7 |
most specific markers for T-cells | CD2 CD3 |
TCR: recognize peptide antigens displayed by MHC | alpha/beta TCR |
TCR: invariant; involved in transduction | CD3 Zeta chain dimer |
TCR: recognize peptides, lipids, small molecules, w/o requirement for display by MHC | gamma/delta TCR |
promote B cell switching to plasma cells to produce IgE; further activation of more CD4+ cells to become TH2 cells (interleukin?) | IL-4 |
most potent eosinophil activator (interleukin?) | IL-5 |
aids in IgE production (interleukin?) | IL-13 |
HLA-B27 | Ankylosing spondylitis, psoriasis, inflammatory bowel disease |
HLA-B8 | Grave's, SLE |
HLA-DR2 | MS, SLE, Goodpasture's |
HLA-DR3 | DM, SLE |
HLA-DR4 | RA, DM Type I, Pehmphigus vulgaris |
HLA-DR5 | Pernicious anemia, Hashimoto's thyroiditis |
HLA-DQ3 | Alopecia areata |
graft rejection: preformed antibody causing immediate vascular injury via ADCC | Hyperacute Rejection |
graft rejection: days, months, years later; via T-cell mediated cytotoxic damage | Acute Cellular Rejection |
kidney rejection: early: subendothelial inflamm & hypertrophy of endothelium; intermediate: moderate intimal prolif. w/ more significant wall inflamm; severe: significant fibrinoid necrosis & intimal prolif.; via cell-mediated & humoral immunity | Acute Vascular Rejection |
kidney rejection: intimal fibrosis w/ vascular thickening; mononuclear infiltrates w/ prominent plasma cells; hyalinized stroma; both T-cell and humoral mechanisms | Chronic Rejection |
cell necrosis of skin & GIT, cholestasis (phase of GVHD) | Acute Phase |
over 100 days post-transplant dermal fibrosis, desquamative esophagitis, portal tract fibrosis, cholestasis (phase of GVHD) | Chronic Phase |
organs prominently involved in GVHD | liver, intestine, skin |
marked cholestasis, yellow-green bile pigment; jaundice, fine scaling rash, vacuolization of epidermal cells | Graft-vs-Host Disease |
most common cause for liver transplantation in children | Biliary Atresia |
Histocompatability required in what organs? | kidney, bone marrow |
w/in 2mos; mixed inflammatory portal and central vein infiltrates (liver rejection) | Acute Rejection |
continued inflammation, portal fibrosis, arteriolar thickening, bile ductular necrosis (liver rejection) | Chronic Rejection |
heart transplant: lymphocytic infiltrates, possible myocardial fiber necrosis | Acute Cellular Rejection |
heart transplant: immunoglobulin deposition in small arteries = vasculitis | Acute Vascular Rejection |
rim pattern fluorescence | anti-dsDNA, anti-nuclear envelope proteins; SLE |
speckled pattern fluorescence | extractable nuclear antigen; Mixed Connective Tissue Disease |
nucleolar pattern fluorescence | anti-nucleolar RNA; progressive Systemic Sclerosis |
centromere pattern fluorescence | anti-centromeric protein; CREST |
SLE antibodies | anti-dsDNA anti-Smith anti-cardiolipin |
Drug-induced SLE antibody | Anti-histone |
Sjörgen's Syndrome antbody | Anti-SS-A, Anti-SS-B |
PSS Antibody | Anti-DNA-topoisomerase I (Scl-70) |
Polymyositis Antibody | Anti-histidyl-tRNA synthetase (Jo-1) |
MCTD antibody | Anti-ribonucleoprotein |
malar skin rash, discoid skin rash, photodermatitis, serositis, glomerulonephritis, cytopenias, arthralgias, myalgias, vasculitis, dec C1q, thrombosis | SLE |
genes associated w/ SLE | HLA DR-2, DR-3 |
drugs that can produce SLE | Procainamide, Hydralazine, Isoniazid, D-Penicillamine |
skin plaques w/ varying degrees of edema, erythema, scaliness, follicular plugging, skin atrophy surrounded by elevated erythematous border; usually affect face and scalp; no renal involvement | Discoid Lupus Erythematosus |
SLE: what part of the skin is involved? | Dermal-epidermal junction |
skin: chronic inflammatory infiltrates, vasculitis, vacuolization and dissolution of epidermis, purpura w/ RBC extravasation into upper dermis | SLE |
SLE: immune complexes seen in dermal epidermal junction? | IgG, C3 |
vascular thrombosis in dermis; in vitro: interfere w/ coagulation; in vivo: hypercoagulable, recurrent arterial & venous thrombosis, fetal loss | Antiphospholipid Syndrome |
APS: autoantibodies directed against? | anionic phospholipids; cardiolipin |
glomerulus: thickened capillary loops, "wire loop" capillaries, surrounding renal tubules are unremarkable | Lupus Nephritis |
high titers of antibodies to ribonucleoprotein particle-containing U1 ribonucleoprotein | MCTD |
modest renal involvement, pulmonary hypertension, interstitial lung disease; overlap of SLE, scleroderma, polymyositis | MCTD |
calcinosis, Raynaud's phenomenon, esophageal dysmotility, sclerodactyly, telangectiasis; associated malabsorption -> riboflavin deficiency -> cheilosis | Limited Scleroderma/ CREST Syndrome |
renal arterial intimal thickening and proliferation; hyperplastic arteriosclerosis -> malignant HPN w/ arterial fibrinoid necrosis, thrombosis & renal infarction | Diffuse Scleroderma |
diffuse alveolar fibrosis = honeycomb fibrosis; morphea | Diffuse Scleroderma |
symmetrical inflammation of skeletal muscle w/ weakness; skin rash; heliotropic rash | Polymyositis-Dermatomyositis |
fibrosis of lacrimal and salivary gland, xerostomia | Sjörgen's Syndrome |
lacrimal and salivary gland inflammation of any cause | Mikulicz's Syndrome |
failure of B cell precursors to develop into mature B cells | X-linked Agammaglobulinemia/ Congenital Agammaglobulinemia/ Bruton's Disease |
inheritance of Bruton's Disease | X-linked recessive |
Bruton's Disease: genetic defect involved? affect production of? | Xq21,22 Bruton tyrosine kinase, btk |
absent B-cells, intact T-cell immunity; multiple infections w/ bacterial organisms; not apparent until about 6mos | Bruton's Disease |
normal numbers of circulating B cells; hyperplastic germinal centers; NO plasma cells | Common Variable Immunodeficiency |
impaired secretion of on or more Ig (usually IgG, IgA); selective abnormality of T cell activation (dec synthesis of IL-2, 4, 5) | Common Variable Immunodeficiency |
dec. in CD4 cells or increase in CD8 cells; presence of T and B cell autoantibodies | Common Variable Immunodeficiency |
genetic defect in DiGeorge Syndrome | specific deletion of 22q |
field defect of 3rd and 4th pharyngeal pouch development in utero | DiGeorge Syndrome |
total absence of thymic tissue; hypocalcemia, seizures | Complete DiGeorge Syndrome |
slight dec. in peripheral T cells; inc. infections but w/ less frequency and severity; hypocalcemia, seizures | Partial DiGeorge Syndrome |
very little serum IgG, virtually no IgM or IgA | SCID |
defect in X-linked SCID: mutation? | mutation in Xq = defective gamma chain of IL-2 receptor |
Autosomal Recessive SCID: defect? | lack of adenosine deaminase (ADA) = impaired purine metabolism |
infants develop: candidiasis, persistent diarrhea, severe respi tract infection w/ Pnuemocystis carinii, Pseudomonas, failure to thrive after 3mos | SCID |
inheritance of Wiskott-Aldrich Syndrome? | X-linked recessive |
thrombocytopenia, eczema, dec IgM, inc IgA & igE; T-cells: cytoskeletal disorganization, loss of microvilli, little CD43 | Wiskott-Aldrich Syndrome |
genetic defect in Ataxia Telangiectasis? | 11q; predisposes to chromosome breakage & rearrangement on chromosomes 7 & 14 |
inheritance of Ataxia Telangiectasia | Autosomal recessive |
progressive cerebellar ataxia, mucocutaneous telangiectasia, recurrent respi tract infection | Ataxia Telangiectasia |
lack circulating and secretory IgA; impaired survival of IgA producing plasma cells | Selective IgA deficiency |
develop anti-IgA antibodies of the IgE type | Selective IgA deficiency |
giant cytoplasmic granules; leukopenia (what disorder? inheritance?) | Chediak-Higashi Syndrome autosomal recessive |
defect in Chronic Granulomatous Disease? | lack of NADPH oxidase |
macrophage-rich chronic inflammatory reaction; susceptibility to catalase-positive agents | Chronic Granulomatous Disease |
profound suppression of T-cell mediated immunity, opportunistic infection, secondary neoplasm, neurologic disease | AIDS |
major targets of HIV infection | T helper cells, Macrophages, Monocytes, Dendritic cells |
lymphopenia, dec T cell function in vivo & vitro, polyclonal B cell activation, altered monocyte/macrophage function | AIDS |
Viremia; sore throat, myalgias, fever, rash, weight loss, fatigue, cervical adenopathy, diarrhea, vomiting; resolves spontaneously (what phase?) | Acute Retroviral Syndrome |
persistent lypmhadenopathy w/ fever, rash, fatigue; period of clinical latency (what phase?) | Middle Chronic Phase |
fever of more than 1 month duration, fatigue, weight loss, diarrhea, serious opportunistic infection, secondary neoplasms, clinical neurologic disease (what phase?) | Final/Full Blown Progression to AIDS |
CDC HIV: Category 1 | greater than or equal to 500cell/uL |
CDC HIV: Category 2 | 200-499 cell/uL |
CDC HIV: Category 3 | < 200 cells/uL |
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