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Immunology

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drnieves's version from 2017-06-20 13:03

Section

Question Answer
EosinophilsType 1 hypersensitivity + ADCC
Local defense against CandidiasisT cells
Systemic candidiasis prevented byNeutrophils
SCIDDefecitive IL-2 R y-chain (X), adenosine deaminase deficiency (AR), RAG 1,2 nonsense mutation.
SCID sxfailure to thrive, chronic diarrhea, trush. Decrease in T cell excision cycles, no thyme shadow, germinal centers or T cells.
Bone marrow transplantSCID tx
Wiskott- AldrichXR
B and T cell disordersSCID, Wiskott-Aldrich, ataxia talangiectasia, Hyper IgM syndrome
Was gene mutation. T can't recognise actinWiskott-Aldrich
Wiskott AldrichThrombocytopenic purpura, eczema, infections, fever, smaller platelets.
High IgE, IgAWiskott-Aldrich
Ataxia talangiectasiaATM gene mutation can't repair DNA double strand and goes to cell arrest.
Ataxia, spider angiomas, low IgA, IgE, IgG, high AFP ataxia talagiectasia sx
ataxia talangiectasia: lymphopenic, cerebellar atrophyataxia talangiectasia
Hyper IgM syndromeDefective CD40 L on Th leading to a class switching problem.
Pyogenic infections, opportunisticHyper IgM syndrome
High IgM, other Ig lowHyper IgM syndrome
GranulomaForeign bodies can produce one.
Form of chronic inflammation characterised by aggregates of activated macrophages that assume epithelioid appearanceGranuloma
L selectinBinds E/P selectin on endothelial cells. Rolling
CD18 B 2 integrins (Mac-1 and LFA-1)tightly binds ICAM-1
TransmigrationPECAM-1
Type 3Deposition of immune complexes. Complement activation. Neutrophils
PSGN, lupus nephritis, serum sickenessType 2
Fever, pruritic rash, arthralgias, low C3 and C4type 3
INF-y deficiencymycobacterial disease in childhood.
Type IICytotoxic (ab mediated). IgM, IgG bind ag.
3 mechanisms: Opsonisation and phagocytosis, complement and Fc R, ab mediated cellular dysfunctionType II
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