Immunology

Innate and adaptive immunity, hypersensitivity, immunodeficiency and transplant rejection — heavily tested with mechanism-first questions.

Exam weight 6–9% · 2 QBank items · 3 flashcards

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Cells & lymphoid organs

T cells mature in the thymus (positive selection in cortex, negative selection in medulla); B cells mature in bone marrow.
MHC I presents endogenous peptides to CD8; MHC II presents exogenous peptides to CD4 — 'rule of 8'.
NK cells kill targets lacking MHC I and are enhanced by IL-2, IL-12 and IFN-α/β.
Spleen filters encapsulated organisms — asplenia demands vaccination against S pneumoniae, H influenzae and N meningitidis.

'Hot T-bone stEAk': IL-1 fever, IL-2 T-cell growth, IL-3 bone marrow, IL-4 IgE, IL-5 IgA/eosinophils, IL-6 acute phase.
C3 deficiency: severe recurrent pyogenic sinopulmonary infections; C5–C9 deficiency: recurrent Neisseria.
C1 esterase inhibitor deficiency causes hereditary angioedema — ACE inhibitors are contraindicated.
Deficient GPI anchors (DAF/CD55, CD59) cause paroxysmal nocturnal hemoglobinuria; treat with eculizumab.

Type I: IgE-mediated, immediate — anaphylaxis, atopy; tryptase rises.
Type II: antibody against fixed tissue antigen — autoimmune hemolytic anemia, Goodpasture, myasthenia gravis; positive direct Coombs.
Type III: immune complexes — serum sickness, SLE nephritis, post-streptococcal glomerulonephritis; low complement.
Type IV: T-cell mediated, delayed — PPD, contact dermatitis, transplant rejection; no antibody involved.

Bruton agammaglobulinemia (BTK, X-linked): recurrent bacterial infection after 6 months, absent B cells and tonsils.
DiGeorge (22q11): tetany from hypocalcemia, absent thymus, conotruncal cardiac defects.
Chronic granulomatous disease (NADPH oxidase): catalase-positive organisms; abnormal dihydrorhodamine flow cytometry.
Hyper-IgE (Job syndrome): coarse facies, cold staphylococcal abscesses, retained primary teeth, eczema.

Hyperacute rejection is minutes and preformed antibody; acute is weeks and cellular; chronic is months–years with fibrosis and vasculopathy.
Graft-versus-host disease: donor T cells attack host skin, gut and liver — classically after bone marrow transplant.
Cyclosporine and tacrolimus inhibit calcineurin — nephrotoxicity; tacrolimus adds neurotoxicity and diabetes, cyclosporine adds gum hypertrophy and hirsutism.
Sirolimus blocks mTOR: not nephrotoxic but causes pancytopenia and hyperlipidemia; useful with renal grafts.