immunology Flashcards
type 4 delayed hypersensitivity reaction moa
doesn’t involve antibodies or complement; occurs 1-2 days after exposure as antigen is taken up by dendritic cells, displayed on MHCII, and stimulate Th1 to release interferon-gamma and attract MO
reactive arthritis triad, age group, and lab finding
urethritis, arthritis, and conjunctivitis; young men; HLA-B27
hep B markers of DNA replication
HBeAg, HBV DNA
hep B chronic infection lab findings
high HBeAg, low anti-HBeAg
eosinophil 2 functions
- defense against parasites: IgE detects parasites, binds and attracts eosinophil via IgE FcR, euosinophil releases major basic protein to kill parasite; 2. regulate type 1 hypersensitivity rxn (mediated by mast/basophils): by releasing histaminase, which helps reduce severity of atopic reaction
EBV nydus of infection
pharyngeal mucosa and tonsillar crypts, then blood
EBV binds to what receptor on what cell?
CD-21 (C3d complement receptor) on mature B-cells
EBV histological giveaway
CD8+ cells that clinically expand to destroy the virus-infected cells; appear much larger with lots of cytoplasm, eccentrically placed nucleus, and cell membrane that conforms to nearby cell bodies
monocotyes and macrophages: signals identity and serves as LPS receptor
CD14
type 1 hypersensitivity: moa
initial exposure: develop a wheal and undergo class-switching to IgE specific to antigen; re-exposure will result in cross-linking on the surface of basophils and mast cells, degranulation, and release of histamine, proteases, leukotrienes, prostaglandins, and heparin
TNF-alpha produced by what cells, does what, and is elevated in what diseases?
mast cells and macrophages; activation of inflammatory cells (CD4, PMN, fibroblasts, endothelial cells) and apoptosis of tumor cells; increased in inflammatory conditions like RA, psoriatic arthritis
Anti-TNF-alpha IG
infliximab, eternacept
toxic shock syndrome moa
superantigen that activates large numbers of helper T-cells (release IL-2) and MO (release IL-1 and TNF); cause capillary leakage, circulatory collapse, hypotension/shock, fever, and skin findings
TB: mycobacteria survival strategy
hide in MO, able to escape killing and replicate w/i phagollysozomes
TB: macrophage response
- present antigen to naive Th cells, 2. secrete IL-12 to induce Th1 differentiation (to produce interferon gamma to help MO), and 3. produce TNF-alpha to recruit additional MO to wall bacteria in
TB: histological hallmark
epithelioid MO
hep C genetic variation: 2 moa
hypervariable region for envelope glycoprotein; no proofreading 3’-5’ exonuclease activity on virion-encoded RNA polymerase
chronic granulomatous dz: moa, pw, dx
inactivation of NADPH oxidase leads to decreased oxidative burst and impaired phagocytic intracellular killing; pw recurrent infection with coag + bacteria, lungs, skin, LN, liver involved, w/ diffuse granulomatous formation; dx by measuring PMN superoxide products (DHR flow cytometry or nitroblue tetrazolium test)
Dihydrorhodamine flow cytrometry test
measures conversion of DHR to rhodamine (fluorescent green); decreased NADPH activity, decreased fluorescence
Nitroblue tetrazolium test
NADPH oxidaises yellow NBT to dark blue; if yellow, then dz positive
What disease presents similarly to chronic granulomatous disease?
myeloperoxidase deficiency (normal DHR/NBT test)
Chediak-higashi syndrome: moa, pw
AR defect in phagosome-lysosome fusino in PMN, leading to abnormal giant lysosomal inclusions visible on light microscopy; pw recurrent pyogenic infectino by strap, strep, albinism, neurological defects (nystagmus, neuropathy)
NK cell (10 percent of all lymphocytes): function, moa
destroy cells w decreased/absent MHCI (virus, tumor); release perforins that punch holes in membranes and granzymes that induce target cell apoptosis
NK cells surface markers
CD16, CD56