IgMPentamer (5 units); first antibody produced; best complement activator; primary response
IgADimer with secretory component; found in gut, saliva, breast milk, tears; mucosal immunity
IgEBinds Fc receptors on mast cells and basophils; mediates allergy and antiparasitic immunity
IgDMainly a B-cell surface receptor; function in serum not well understood
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🛡️ Immunology · MHC
MHC I: ALL nucleated cells → CD8+. MHC II: APCs only → CD4+. Memory: "1×8=8, 2×4=8."
MHC (HLA) — MHC I (HLA-A,B,C) on all nucleated cells presents to CD8+ · MHC II (HLA-DR,DP,DQ) on APCs presents to CD4+
How the immune system reads what is inside every cell in the body
MHC I: displays intracellular peptides (viral proteins, tumor antigens) to CD8+ CTLs. All nucleated cells express MHC I — this is how we identify infected/cancerous cells. MHC II: on dendritic cells, macrophages, B cells only. Displays extracellular antigens after phagocytosis → CD4+ T cell activation. Transplant rejection = MHC mismatch.
Type I (A)Anaphylactic — IgE bound to mast cells; antigen crosslinks → histamine release; immediate (minutes)
Type II (C)Cytotoxic — IgG/IgM bind cell surfaces → complement + phagocytosis; AIHA, Goodpasture's, Graves'
Type III (I)Immune complex — Ag-Ab complexes deposit in tissues → complement → inflammation; SLE, serum sickness, PSGN
Type IV (D)Delayed/cell-mediated — T cells (no antibody); 48-72 hr; PPD test, contact dermatitis, transplant rejection
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🛡️ Immunology
B cell activation: Signal 1 (antigen) + Signal 2 (CD40L-CD40 + cytokines) → class switch IgM→IgG/IgA/IgE
B Cell Activation and Class Switching — two signals required; Signal 1=antigen binds BCR · Signal 2=CD4+ Th2 provides CD40L→CD40 + cytokines
How B cells become antibody-secreting plasma cells — and why two signals are required
Signal 1: antigen binds B cell receptor (BCR). Signal 2: CD4+ Th2 cell provides CD40L → CD40 contact + cytokines (IL-4, IL-5, IL-13). Without signal 2 → anergy (tolerance). Class switching: IgM → IgG/IgA/IgE driven by cytokines. Affinity maturation in germinal centers. Memory B cells persist for rapid secondary response.
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Flashcard
🃏 🛡️ Immunology
B cell activation — the two signals?
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🃏 Answer
B cell activation: Signal 1 (antigen) + Signal 2 (CD40L-CD40 + cytokines) → class switch IgM→IgG/IgA/IgE
B Cell Activation and Class Switching — two signals required; Signal 1=antigen binds BCR · Signal 2=CD4+ Th2 provides CD40L→CD40 + cytokines
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🛡️ Immunology · Innate
NK cells kill cells that LACK MHC I — "missing self." No prior sensitization needed.
Natural Killer Cells — innate lymphocytes that detect "missing self" (absent MHC I) and kill by releasing perforin and granzymes
The innate immune cells that hunt virus-infected and tumor cells
NK cells have activating receptors (NKG2D — detect stress ligands) and inhibitory receptors (KIR — check for MHC I). Viruses downregulate MHC I to hide from CTLs → this exposes them to NK cells. Activated NK: perforin creates pores + granzymes induce apoptosis. Enhanced by IL-2, IL-12, interferons.
Immunological Memory — primary exposure creates memory B and T cells; secondary exposure produces faster, stronger IgG-dominated response
Why the second infection produces stronger protection — the basis of vaccination
First exposure: naïve cells activated → 1–2 week lag. IgM predominates. Low antibody titer. Memory B and T cells formed. Second exposure: memory cells respond within hours-days. Predominantly IgG (high affinity, class-switched). Much higher titer, longer duration. Vaccines use prime + boost strategy to exploit this mechanism.