Autoimmunity after streptococcal infection – tissue cross-reactivity Cell wall protein (M protein) of Streptococcus pyogenes exhibits antigenic mimicry and can cross-react primarily with which human tissue?

Introduction / Context:
Post-streptococcal autoimmune complications result from molecular mimicry. M protein, a major virulence factor of S. pyogenes, is central to rheumatic carditis through cross-reactivity with cardiac tissues.

Given Data / Assumptions:

• Focus here is specifically on protein (M protein) cross-reactivity, not group carbohydrate.
• Potential target tissues include myocardium and valves.

Concept / Approach:

Antibodies to M protein cross-react with myocardial tissue and sarcolemmal antigens, contributing to pancarditis. Although valvular damage is prominent clinically, the classic exam pairing for M protein is myocardium; carbohydrate antigens are often linked to valvular reactivity.

Step-by-Step Solution:

Verification / Alternative check:

Immunohistochemical studies demonstrate anti-M protein antibodies binding to heart muscle fibers; animal models reproduce myocarditis after immunization with M protein fragments.

Why Other Options Are Wrong:

• Cardiac valves: frequently affected clinically but more strongly associated in exams with group carbohydrate mimicry.
• Synovial fluid/Vascular intima/Hepatic tissues: not primary targets of M protein cross-reactivity.

Common Pitfalls:

• Conflating different streptococcal antigens and their human targets; exam questions often split protein vs. carbohydrate.

Final Answer:

Myocardium