Pathology · Chapter 3
Immunopathology
The chapter question
When the immune system injures a tissue, which clues tell you the mechanism, and why does the mechanism decide the test and the treatment?
Type I · Immediate
- Target
- Free antigen meeting IgE on mast cells
- Effector
- Histamine, tryptase, lipid mediators
- Injury
- Leak, bronchospasm, itch
- Clue
- Minutes; wheal; tryptase
Type II · Antibody
- Target
- Antigen fixed on a cell or matrix
- Effector
- IgG/IgM + complement, phagocytes, NK; or a receptor
- Injury
- Lysis, removal, inflammation, receptor on/off
- Clue
- Coombs+; linear IF
Type III · Immune complex
- Target
- Complexes formed in blood
- Effector
- Deposition, complement, neutrophils
- Injury
- Vasculitis, GN, arthritis
- Clue
- Granular IF; low C3/C4
Type IV · Delayed
- Target
- Peptide on MHC (no antibody)
- Effector
- Th1 → macrophages; CD8 killing
- Injury
- Induration, granuloma, cell death
- Clue
- 48–72 h; lymphocytes
Make a quick prediction
A 9-year-old boy has puffy eyes and cola-colored urine two weeks after a strep throat. What is most likely damaging his glomeruli?
Study path
Follow the order or jump to the concept you need. Every topic has a Deep Learning and a High-Yield view of the same facts, and ends with a short knowledge check.
0 of 7 topics studied0 of 55 questions correct
- 3.120 minUp nextImmune recognition: innate and adaptiveInnate cells recognize shared danger patterns within minutes; lymphocytes recognize one antigen each, after days, and remember it. Every immunopathology in this chapter is one of these systems aimed at the wrong target, too hard, or too weakly.Two systems, two kinds of recognitionPAMPs, DAMPs, TLRs and the inflammasomeImmune privilegeActive or passive, natural or artificial+1
- 3.224 minAntigen presentation, T-cell help and antibodiesT cells see only peptide displayed on MHC. Where a protein came from decides which MHC shows it and which T cell answers; costimulation decides whether the answer is attack or tolerance; T-cell help decides which antibody class a B cell makes.MHC class I and class II: two routes to the surfaceHLA genes on chromosome 6Two signals: activation, anergy and class switchingHelper subsets: Th1, Th2, Th17 and Treg+2
- 3.338 minHypersensitivity reactionsHypersensitivity is a normal immune mechanism doing harm. Read every case in the same order: what triggered it, where the antigen sits, which effector did the damage, what injury resulted, and which clue in the case proves it.One method for four typesHypersensitivity case sorterType I: IgE and mast cellsType II: antibody against a fixed antigen+3
- 3.418 minTransplantation immunologyA graft is a large, foreign HLA antigen. Whether it is destroyed in minutes, weeks or years depends on what the recipient already has (preformed antibody), what it makes next (T cells and new antibody), and in which direction the attack runs.Graft typesMatching: ABO, HLA and the crossmatchRejection: minutes, weeks or yearsGraft-versus-host disease and graft-versus-leukemia
- 3.530 minAutoimmune diseaseSelf-reactive lymphocytes are made every day. Autoimmune disease follows when the checks that delete, silence or suppress them fail in a genetically susceptible person and something in the environment sets them off. The injury then uses the same hypersensitivity mechanisms as any other immune attack.Tolerance and how it failsSystemic lupus erythematosus: mechanism and manifestationsAutoantibodies and laboratory testsAntiphospholipid syndrome: the clotting paradox+1
- 3.624 minPrimary immunodeficienciesEach inherited immunodeficiency removes one part of the system, and the infections that follow are the ones that part normally controls. Read every case as defect → infection pattern → lab clue.Reading a defect from its infectionsB-cell defects: Bruton, selective IgA, CVIDT-cell defects: DiGeorge, IL-12 receptor, Job, mucocutaneous candidiasisCombined and syndromic defects: SCID, ataxia–telangiectasia, hyper-IgM, Wiskott–Aldrich+1
- 3.732 minHIV, complement disorders and amyloidosisThree ways the immune system fails beyond the inherited lymphocyte defects: a virus that destroys the CD4 cells everything else depends on; missing complement components or regulators; and chronic immune activity that leaves misfolded protein in the tissues.HIV: genes, transmission, entry and drug targetsWhy CD4 cells disappear, and where the virus hidesStages, tests, opportunistic infections and tumorsComplement deficiencies: early, central, terminal and regulators+2
Practice
Interactive labThe hypersensitivity case sorter, The Missing Arrow, Almost Twins and One Fact Changes. Each also appears inside the topic where it helps most.High-yield cards40 cards on clues, comparisons and mechanisms worth recalling.Chapter reviewBringing it together: one disease, three mechanisms, then 16 mixed case-based questions with explanations.Case and source mapWhat each supplied case and lecture question tests (42 items), linked to where it is practised, with the source page map.
How the ideas connect
14 bridges carry one concept into the next, within this chapter and across chapters. Each is taught where you first need it.
- Recognition → presentation → hypersensitivity3.3 · Hypersensitivity case sorter
- Tolerance failure → autoimmunity3.5 · The Missing Arrow
- HIV entry → CD4 depletion → opportunistic infection3.7 · Why CD4 cells disappear
- Th1–macrophage axis → granuloma3.2 · Granuloma bridge
- Caseous necrosis (Chapter 1)1.6 · Caseous necrosis
- Fibrinoid necrosis in vasculitis (Chapter 1)1.6 · Fibrinoid necrosis
- Cytotoxic T-cell killing (Chapter 1)1.7 · Cytotoxic T cells
- Amyloid structure and types (Chapter 1)1.8 · Amyloid
- Granulomatous inflammation (Chapter 2)2.6 · Chronic and granulomatous inflammation
- Leukocyte adhesion deficiency (Chapter 2)2.2 · Leukocyte recruitment
- CGD and Chédiak–Higashi (Chapter 2)2.3 · Phagocytosis and killing
- Antiphospholipid syndrome → thrombosis (Chapter 4)4.6 · Thrombosis and embolism
- DiGeorge 22q11 deletion (Chapter 5)5.2 · Chromosomal syndromes
- ATM, immunodeficiency and lymphoma (Chapter 7)7.4 · Epidemiology and genetics