Complement

5 ASCP MLS practice questions on Complement, part of Immunology. The first 5 are below; the first 5 with answers and explanations (tap Show answer after you have chosen), the rest in Learn with a free account.

1. Question 1 · Hard

   A 19-year-old has a second episode of meningococcal meningitis. CH50 and AH50 are both undetectable, while C3 and C4 are normal. Which deficiency is most likely?

   1. AA terminal component, C5 to C8
   2. BA regulator, C1 inhibitor
   3. CAn early classical component, C2
   4. DAn alternative pathway protein, properdin

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   Answer: A · A terminal component, C5 to C8

   CH50 tests the classical pathway and AH50 the alternative pathway, and both need C5 to C9 to lyse the target cells. When both are absent but C3 and C4 are normal, the defect lies in a shared terminal component. People lacking C5 to C9 cannot form the membrane attack complex and have recurrent Neisseria infections. In C9 deficiency some lysis still occurs, so the CH50 is low rather than absent.

   • B: C1 inhibitor deficiency causes angioedema with a low C4, not absent CH50 and AH50.
   • C: C2 deficiency removes CH50 activity but leaves AH50 normal.
   • D: Properdin deficiency lowers AH50 but leaves CH50 normal.

2. Question 2 · Easy

   Which complement fragment is the most potent anaphylatoxin and attracts neutrophils?

   1. AC5a
   2. BC4b
   3. CC5b
   4. DC3b

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   Answer: A · C5a

   C5a is the strongest anaphylatoxin, more potent than C3a; both make mast cells release histamine and increase vascular permeability. C5a is also a powerful chemoattractant for neutrophils and monocytes. C3b is the main opsonin, and C5b starts assembly of the membrane attack complex with C6 to C9. The small 'a' fragments mainly drive inflammation, while most large 'b' fragments bind to surfaces.

   • B: C4b forms part of the classical and lectin C3 convertase.
   • C: C5b starts the membrane attack complex.
   • D: C3b coats microbes as the main opsonin.

3. Question 3 · Medium

   Which complement results are typical of hereditary angioedema caused by C1 inhibitor deficiency?

   1. ALow C4, normal C3
   2. BNormal C3 and C4, low factor B
   3. CLow C3, normal C4
   4. DLow C3 and low C4

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   Answer: A · Low C4, normal C3

   Without enough C1 inhibitor, C1 is activated unchecked and keeps cleaving C4 and C2, so C4 is low even between attacks while C3 stays normal. The swelling itself is caused by bradykinin, because C1 inhibitor also controls kallikrein in the contact system; this is why antihistamines do not help. A low C4 is a good screening test, followed by C1 inhibitor level and function. In type II disease the protein level is normal but its function is low.

   • B: Factor B is used up in alternative pathway activation, not in C1 inhibitor deficiency.
   • C: Low C3 with normal C4 suggests alternative pathway activation, as with C3 nephritic factor.
   • D: Low C3 and C4 together suggest classical activation by immune complexes, as in active SLE.

4. Question 4 · Easy

   In the lectin pathway, mannose-binding lectin bound to microbial sugars activates complement through:

   1. AFactor B cleaved by factor D
   2. BDirect cleavage of C5 by properdin
   3. CThe C1q, C1r and C1s complex
   4. DMBL-associated serine proteases (MASPs)

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   Answer: D · MBL-associated serine proteases (MASPs)

   Mannose-binding lectin and ficolins recognize sugar patterns on microbes and carry MBL-associated serine proteases (MASP-1 and MASP-2). MASP-2 cleaves C4 and C2 to form the same C3 convertase as the classical pathway, C4b2a. No antibody is needed, so the lectin pathway is part of innate immunity. The classical pathway uses C1q, C1r and C1s, and the alternative pathway uses factors B and D.

   • A: Factors B and D belong to the alternative pathway.
   • B: Properdin stabilizes the alternative pathway C3 convertase; it does not cleave C5.
   • C: C1q, C1r and C1s start the classical pathway, usually after antibody binds.

5. Question 5 · Medium

   Which complement pathway begins when C1q binds to antigen-antibody complexes containing IgM or IgG?

   1. AThe membrane attack pathway only
   2. BThe alternative pathway
   3. CThe lectin pathway
   4. DThe classical pathway

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   Answer: D · The classical pathway

   The classical pathway starts when C1q binds the Fc region of antibodies attached to antigen; IgM is the most effective. C1r and C1s then cleave C4 and C2 to form the C3 convertase. The alternative pathway starts on microbial surfaces without antibody. The lectin pathway starts when mannose-binding lectin binds carbohydrates on microbes.

   • A: The membrane attack complex is the shared final step, not a starting point.
   • B: The alternative pathway does not need antibody to start.
   • C: The lectin pathway starts with mannose-binding lectin, not C1q.