Immunopathology: early classical complement deficiency: practice question

A Pathology question in the style of the NEET PG paper. Answer it first, then read why the right option is right and why each of the others is wrong.

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Pathology · Immunopathology: early classical complement deficiency

Sample item

A 20-year-old woman has a malar rash, arthritis and glomerulonephritis, with undetectable total haemolytic complement activity. Genetic testing shows homozygous C1q deficiency. Why does this deficiency predispose to lupus?

Original practice item, not a recalled exam question. Nothing here is recorded.

The answer and the reasoning

B. Apoptotic debris and immune complexes are not cleared

C1q, C2 and C4 help clear apoptotic cells and immune complexes. Their deficiency leaves nuclear antigens exposed, favouring breakdown of tolerance and SLE-like disease. In contrast, terminal component deficiency (C5-C9) predisposes to Neisseria infection.

Option by option

  • A. Helper T cells fail to mature in the thymus

    T-cell maturation in the thymus is not affected by C1q.

  • B. Apoptotic debris and immune complexes are not cleared (correct)

    Correct. Failure to clear apoptotic material exposes self antigens and promotes autoimmunity.

  • C. Mast cells degranulate without antigen

    Mast cell degranulation is an IgE-mediated or direct event, unrelated to C1q.

  • D. Neisserial infections are no longer controlled

    Neisserial susceptibility follows terminal complement (C5-C9) deficiency.

Source note: Original NextPrep sample item — pending expert review. This item is original practice material awaiting independent expert review, so confirm important facts in a standard textbook.

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Questions about this Pathology question

What is the answer to this Pathology question?

The best answer is B, Apoptotic debris and immune complexes are not cleared. C1q, C2 and C4 help clear apoptotic cells and immune complexes.

Why is "Helper T cells fail to mature in the thymus" not the answer?

T-cell maturation in the thymus is not affected by C1q.

Why is "Mast cells degranulate without antigen" not the answer?

Mast cell degranulation is an IgE-mediated or direct event, unrelated to C1q.

Why is "Neisserial infections are no longer controlled" not the answer?

Neisserial susceptibility follows terminal complement (C5-C9) deficiency.

What concept does this question test?

It tests Immunopathology: early classical complement deficiency in Pathology. Their deficiency leaves nuclear antigens exposed, favouring breakdown of tolerance and SLE-like disease. In contrast, terminal component deficiency (C5-C9) predisposes to Neisseria infection.

How hard is this question?

We tag it as a multi-step question: it asks you to combine more than one idea. The tag is our own editorial judgement, not an official difficulty rating, so read the reason for every option, not only the answer.

How should I study Immunopathology: early classical complement deficiency?

Learn each disease as a bundle: cause, key histology, markers, and the clinical hallmark. Then use the flashcards and the other Pathology questions on this site to test what stuck.

Is this a real NEET PG question?

No. It is an original practice item (editorial status: sample, version 1). NextPrep does not publish recalled or leaked questions, and independent faculty review of this item has not been completed yet, so confirm important facts in a standard textbook.