22.5 Antibodies, Adaptive Immunity and Memory

Three short movements: the case, the anatomyThe study of the structure of the human body. and physiologyThe study of how the body functions., then the tie back to Stina. Each links to the scene where you’ll see it move.

I · Normal, six times

Six ANAs across eleven years, four rheumatoid factors, an anti-dsDNA, an anti-CCP, an ANCA: all negative. Complement normal or high, as in any inflammation. Immunoglobulins in range. The 2015 electrophoresis found one thing — a small sharp spike, one clone of plasma cellsImmune cells that develop from B cells and produce antibodies. making one antibody, called MGUS because it caused no symptoms and nobody could say what it meant; oncology has tracked it since. “Autoimmune workup negative,” the chart says, and files it under reassurance. This chapter is about why it is the most informative result she has.

See it move: Scene 1 · Hey, I Found This · Scene 5 · The Clean Panel

II · Antigen, MHC, and the T cell’s school

The adaptive arm recognises faces, not patterns. An antigen is anything that can be recognised; the part seen is an epitope, a few amino acids or sugars; a hapten (poison ivy, nickel) is too small alone and rides a body protein. T cellsThe basic structural and functional units of life. see antigen only on an MHC molecule — the HLA genes on chromosome 6, the most polymorphic in the body, the reason transplants are matched. Class I, on every nucleated cell, shows what is made inside (a virus, a tumour protein) to CD8 cytotoxic cells; class II, only on the professional presenters — dendritic cell, macrophage, B cell — shows what was eaten to CD4 helpers: “Hey, I found this.” The dendritic cell carries the news to the paracortex, and the lecture’s three signals follow: receptorA structure that detects stimuli. on MHC-peptide, the CD28–B7 handshake that is missing when the presenter is not alarmed, and IL-2 for expansion. Without all three the T cell goes anergic — one way self is tolerated. Helpers come in flavours: Th1 for macrophages and killers, Th2 for antibody, Th17 for neutrophils and the psoriasis the lecture traces through IL-23 and IL-17, and regulatory T cells that shut the rest down with IL-10 and TGF-β. Cytotoxic T cells kill as NK cells do — perforin, granzymes, Fas ligand. The school is the thymus; two percent graduate.

See it move: Scene 1 · Hey, I Found This · Scene 2 · T Cells: Schooled, Signalled, Specialised

III · Antibodies, memory, and what the clean panel means

B cells see native antigen directly and most need a Th2 cell’s help; the activated clone divides into plasmaThe liquid component of blood. cells — all rough ER, a clock-face nucleusThe control center of the cell that contains DNA and directs cellular activities., antibody pouring out for days, a few surviving in the marrow for decades — and memoryThe ability to store and recall information. cells. The antibody is the receptor set loose: two heavy chains (~400 amino acids), two light (~200, kappa or lambda), variable tips that bind, a constant stem read by Fc receptorsProteins located on the surface or inside cells that bind specific molecules (e.g., neurotransmitter and complement. Five classes: IgM, the pentamer, first out, best at fixing complement; IgA, the dimer of secretions; IgD, the naïve receptor; IgG, most of the serum, crosses the placentaThe organ that facilitates nutrient and waste exchange between the mother and fetus., runs the secondary response; IgE, parked on mast cells — the lecture’s blue cheese, Adjani’s peanut. Four jobs: neutralization, agglutinationThe clumping of red blood cells when antibodies bind to their specific antigens., precipitation, complement fixation. The first exposure is slow, small and IgM; the second fast, tall and IgG — memory, the reason a vaccine is a rehearsal, an anaphylaxis needs a second exposure, and chickenpox at seven can return as shingles at seventeen. Active immunity is your own; passive is borrowed (placental IgG, milk IgA, immune globulin) and leaves no memory. When the adaptive arm turns on self — Hashimoto’s, Graves’, celiac, type 1 diabetes, lupus, rheumatoid arthritis, myasthenia — it leaves a signature: autoantibodies, immune complexes in the kidney (type III), gradual onset, a chronic destructive course. The four hypersensitivities are its failure modes: I, IgE on mast cells, minutes; II, IgG on a cell surface; III, complexes in vessels and glomeruli; IV, T cells, days. Her panel has none of it: no autoantibody in eleven years, no complexes in a kidney that showed amyloid instead, onset in hours, tissue intact. The adaptive arm was never shown a self-target; a sterile fire supplies neither antigen nor co-stimulation. The spike is a different sentence — one plasma-cell clone, the second “uncertain significance” in her chart, which the Blood module filed under TEMPI and this module leaves in oncology’s hands.

See it move: Scene 3 · The Antibody, Five Ways · Scene 4 · First Exposure, Second Exposure · Scene 5 · The Clean Panel

5 scenes. Each one has a short animation or a slide, something to explore, a true/false spot-check of your thinking, and a quick check. Every scene gives you an evidence card for your board.

Every scene gave you an evidence card, and the chart adds more. Sort each card into the column it supports: A tolerant, intact adaptive arm — innocent, Neither on its own, or A seronegative autoimmune disease. Some cards can honestly go in more than one place — that’s allowed, and the feedback tells you which cards decide the case.

Time to decide. Look back at your bet, then build your verdict from statements that hold up — no writing needed.