Microbiology Cheat Sheet
Immune Misdirection & Grafts
Hypersensitivity, immunodeficiency and grafts for NEET-PG: Gell and Coombs types, Bruton, CGD, complement deficiency, and graft rejection mechanisms.
MedNext Academy | 3 min read
Immune Misdirection & Grafts
Hypersensitivity, immunodeficiency and grafts for NEET-PG: Gell and Coombs types, Bruton, CGD, complement deficiency, and graft rejection mechanisms.
This topic covers the Gell and Coombs hypersensitivity reactions, primary and secondary immunodeficiency, transplantation immunology, and graft rejection mechanisms.
High-yield lines
- Type I hypersensitivity is IgE-mediated and immediate, occurring within minutes as mast cells degranulate to release histamine and leukotrienes.
- Type II hypersensitivity is antibody-mediated cytotoxicity where IgG or IgM binds cell-surface antigens, seen in autoimmune haemolytic anaemia and Goodpasture syndrome.
- Type III hypersensitivity is immune complex mediated, seen in serum sickness, SLE, and post-streptococcal glomerulonephritis.
- Type IV hypersensitivity is delayed T-cell-mediated, developing over 48 to 72 hours, and the Mantoux tuberculin test is the classic example.
- Serum tryptase is the diagnostic biomarker for anaphylaxis, elevated within 1 to 2 hours of mast cell degranulation.
- B-cell or antibody deficiencies predispose to encapsulated bacteria and recurrent sinopulmonary infections, exemplified by X-linked agammaglobulinaemia (Bruton).
- T-cell deficiencies predispose to intracellular pathogens, viruses, and fungi, exemplified by DiGeorge syndrome with thymic aplasia.
- Chronic granulomatous disease results from defective NADPH oxidase, causing infections with catalase-positive organisms such as Staphylococcus and Aspergillus.
- Terminal complement deficiency of C5 to C9 predisposes specifically to recurrent Neisseria infections.
- Hyperacute graft rejection occurs within minutes due to pre-formed donor-specific antibodies and is prevented by ABO matching and cross-match.
- Acute cellular rejection occurs over days to weeks and is a type IV hypersensitivity mediated by CD4 and CD8 T cells, treatable with pulse steroids.
- Chronic rejection occurs over months to years via the indirect pathway, causing graft arteriosclerosis and irreversible fibrosis.
- Graft-versus-host disease occurs when donor T cells attack an immunocompromised recipient, targeting skin, liver, and GI tract.
- Ankylosing spondylitis has the strongest HLA-disease association with HLA-B27, while coeliac disease is associated with HLA-DQ2 and DQ8.
Mapped competency codes
- MI1.10
- MI1.11
Continue into the full chapter
This summary maps to MI1-general-microbiology-and-immunity.
Frequently Asked Questions
Which hypersensitivity type is the tuberculin (Mantoux) test?
Type IV delayed hypersensitivity, a T-cell-mediated response producing induration read at 48 to 72 hours.
What causes hyperacute graft rejection and how is it prevented?
Pre-formed donor-specific antibodies causing rejection within minutes, prevented by ABO matching and cross-match testing.
Which infections characterise complement C5 to C9 deficiency?
Recurrent Neisseria (meningococcal and gonococcal) infections, because the membrane attack complex cannot form.
What organisms infect patients with chronic granulomatous disease?
Catalase-positive organisms such as Staphylococcus aureus, Aspergillus, Serratia, Nocardia, and Burkholderia, due to defective NADPH oxidase.
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