A physician-validated, board-style question from the Active Transport QBank. Try it, then check the reasoning for every option.
A 19-year-old male is found to have Neisseria gonorrhoeae bacteremia. This bacterium produces an IgA protease capable of cleaving the hinge region of IgA antibodies. What is the most likely physiological consequence of such a protease?
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A
Membrane attack complex formation is impairedIncorrect. IgA does not significantly activate the classical complement pathway or form the membrane attack complex; IgG and IgM are the principal complement-fixing antibodies.
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B
Opsonization and phagocytosis of pathogen cannot occurIncorrect. IgG is the major opsonizing antibody; IgA's main role is mucosal neutralization, not opsonization. Phagocytosis is not the primary IgA function impaired.
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C
Impaired adaptive immune system memoryIncorrect. Adaptive immune memory is maintained by memory B and T cells; cleaving secretory IgA does not impair immunological memory.
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D
Impaired mucosal immune protectionCorrect. IgA's primary function is mucosal neutralization. Cleaving IgA at the hinge abolishes its mucosal protective role, allowing pathogens like N. gonorrhoeae to colonize and invade mucosal surfaces.
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E
Decreased IgE-mediated allergic responseIncorrect. IgE mediates type I hypersensitivity (allergy, anaphylaxis) and is functionally distinct from IgA's mucosal role. Cleaving IgA does not affect IgE-mediated responses.
↑ Tap an answer to reveal the reasoning
Answer: D. IgA antibodies are the predominant immunoglobulin at mucosal surfaces. Dimeric secretory IgA is produced by plasma cells in the lamina propria, then transcytosed across mucosal epithelium where it picks up the secretory component, which protects it from proteolytic degradation in mucosal secretions (saliva, tears, gut lumen, respiratory tract, GU tract). At the mucosal surface, IgA neutralizes pathogens by blocking adherence to epithelial cells.
IgA protease, produced by Neisseria gonorrhoeae, N. meningitidis, Streptococcus pneumoniae, and Haemophilus influenzae, cleaves IgA at its hinge region. This separates the antigen-binding Fab fragments from the Fc portion, abolishing IgA's ability to crosslink antigens and neutralize pathogens at mucosal surfaces. The result is impaired mucosal immune protection, which facilitates the organism's colonization and invasion across the mucosa (genitourinary in gonorrhea).
IgA does not significantly activate the classical complement pathway (membrane attack complex) and is not the dominant opsonin (that's IgG). IgA does not mediate adaptive immune MEMORY (that's a function of memory B and T cells). The selective and specific consequence of cleaving IgA is loss of mucosal immune protection.
**Why each option:**
**A.** IgA does not significantly activate the classical complement pathway or form the membrane attack complex; IgG and IgM are the principal complement-fixing antibodies.
**B.** IgG is the major opsonizing antibody; IgA's main role is mucosal neutralization, not opsonization. Phagocytosis is not the primary IgA function impaired.
**C.** Adaptive immune memory is maintained by memory B and T cells; cleaving secretory IgA does not impair immunological memory.
**D.** Correct. IgA's primary function is mucosal neutralization. Cleaving IgA at the hinge abolishes its mucosal protective role, allowing pathogens like N. gonorrhoeae to colonize and invade mucosal surfaces.