Immunity Physiology
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Direct answer
Innate immunity is the fast, non-specific, germline-encoded defence — complement, phagocytes, natural killer cells — that responds within minutes and does not improve with repeat exposure. Adaptive immunity is the slower, antigen-specific response of T and B lymphocytes that matures over days, discriminates self from non-self through MHC restriction, and leaves behind memory cells so the second encounter is faster and stronger. The two systems are not parallel tracks: antigen-presenting cells, complement fragments and cytokines are the bridge that switches an innate reaction into an adaptive one.
What you must remember
- Differential count: neutrophils 50–70%, lymphocytes 20–40%, monocytes 2–8%, eosinophils 1–6%, basophils under 1%; bacterial infections push neutrophilia with a left shift, viral infections lymphocytosis.
- T lymphocytes mature in the thymus — CD4 helpers (MHC II restricted), CD8 cytotoxic (MHC I restricted), and Tregs; B lymphocytes mature in the bone marrow and become antibody-secreting plasma cells.
- MHC I is on all nucleated cells and presents endogenous (viral, tumour) peptides; MHC II is on antigen-presenting cells — dendritic cells (most potent), macrophages, B cells — and presents engulfed extracellular antigen.
- Natural killer cells are large granular lymphocytes that kill without prior sensitisation, recognise cells with low MHC I, and are key against viruses and tumours.
- Immunoglobulins: IgG — most abundant, only one crossing the placenta; IgM — pentamer, first produced, fixes complement best, includes natural ABO antibodies; IgA — secretory dimer of colostrum and mucosa; IgE — mast cell Fc binding in allergy and parasite defence; IgD — receptor on naive B cells.
- Complement: classical pathway activated by IgM or IgG-antigen complexes via C1q, alternative pathway by spontaneous C3 hydrolysis on microbial surfaces; C3b opsonises, C5b-9 forms the membrane attack complex.
- Neutrophil killing needs the NADPH oxidase oxidative burst — its absence is chronic granulomatous disease; myeloperoxidase generates hypochlorous acid.
- Memory is the adaptive hallmark: primary antibody response peaks IgM in days, secondary response switches to IgG within 24–72 hours with a 10–100-fold titre rise — the physiological basis of vaccination.
Ten days at a wound, from neutrophil to memory cell
Pinprick a finger and watch the timeline. Within minutes, complement fragments and tissue macrophage cytokines dilate vessels; neutrophils marginate along the endothelium, roll on selectins, squeeze through the wall (diapedesis) and follow chemotaxins such as C5a and IL-8. They dominate the first 24 hours, ingesting bacteria and killing them with the oxidative burst. Around 48 hours monocytes arrive, differentiate into macrophages, and present digested peptide on MHC II to naive CD4 cells in the draining node — the dendritic cell is the professional courier that carries antigen there.
The adaptive arm now takes over. Helper T cells release IL-2 and expand clonally; B cells that bind the antigen proliferate, class-switch under cytokine instruction, and affinity-mature in germinal centres. Detectable IgM appears around day 5–7, peaking near day 10–14, with IgG arriving later. Most effector cells then die, but memory B and T cells persist for years — on re-exposure, antigen-specific IgG appears within one to three days at high titre, which is why a second encounter with the same organism is usually asymptomatic. Every step of this sequence maps to a drug or disease: corticosteroids blanch the neutrophil influx, diGeorge syndrome lacks the thymic education step, X-linked agammaglobulinaemia lacks B-cell maturation, and HIV destroys the CD4 conductor itself.
High-yield viva angles
Expect three questions. "Why does IgM fix complement better than IgG?" — because its pentameric shape spaces two Fc regions close enough to bind C1q with high affinity. "Why is the newborn protected by IgG and not IgM?" — only IgG crosses the placenta, actively transported during the third trimester, which is also why preterm infants are relatively unprotected. "Why do viral infections cause lymphocytosis while bacterial ones cause neutrophilia?" — intracellular viruses drive T-cell expansion, whereas extracellular bacteria are handled by the neutrophil line; the blood film is therefore a crude but instant immune map.
Frequently asked questions
Which cells present antigen on MHC II molecules?
Dendritic cells, macrophages and B cells present engulfed extracellular antigen on MHC II to CD4 helper T cells.
Why is IgG the only immunoglobulin transferred across the placenta?
Its Fc portion binds a specific placental transport receptor, so third-trimester fetal passive immunity is entirely IgG-mediated.
What is the role of C3b in host defence?
It opsonises microbes by binding their surface while neutrophil and macrophage C3b receptors engulf the coated organism.
Which enzyme deficiency causes chronic granulomatous disease?
NADPH oxidase deficiency, which abolishes the respiratory oxidative burst so phagocytes ingest but cannot kill catalase-positive organisms such as Staphylococcus aureus.
Why is the secondary immune response faster than the primary?
Pre-existing memory cells recognise the antigen immediately, bypassing the naive-cell expansion phase, and class-switched IgG is produced within 24–72 hours.