Post-streptococcal autoimmunity – cross-reactive targets Antibodies to the cell wall carbohydrate of Streptococcus pyogenes demonstrate molecular mimicry and may cross-react with which human tissue?

Introduction / Context:
Molecular mimicry after group A streptococcal infection underlies non-suppurative sequelae. Distinct streptococcal antigens cross-react with human tissues, driving rheumatic carditis and other complications.

Given Data / Assumptions:

• Focus is specifically on antibodies to cell wall carbohydrate (group-specific polysaccharide), not M protein.
• Target tissues listed include cardiac structures and others.

Concept / Approach:

While M protein cross-reacts notably with myocardium and sarcolemmal antigens, antibodies to group A carbohydrate have been implicated in valvular damage by binding to glycoprotein epitopes in cardiac valves, contributing to rheumatic valvulitis.

Step-by-Step Solution:

Verification / Alternative check:

Histopathology of rheumatic heart disease shows valvulitis with immune deposition; immunologic studies demonstrate cross-reactive antibodies to valve tissue glycoproteins after streptococcal infection.

Why Other Options Are Wrong:

• Myocardium: classically linked to anti-M protein rather than carbohydrate epitopes.
• Synovial fluid/Vascular intima/Renal tubules: not primary targets of the carbohydrate mimicry described here.

Common Pitfalls:

• Conflating M protein cross-reactivity (myocardium) with group carbohydrate (valves).

Final Answer:

Cardiac valves