In the seronegative spondyloarthropathies, HLA-B27 antigen association is strong. The molecular mimicry hypothesis proposes that HLA-B27 presentation of which type of microbial antigen triggers autoimmunity?

• A Arthritogenic peptides from Klebsiella, Chlamydia, or Salmonella sharing homology with B27 itself ✓
• B Streptococcal M protein cross-reacting with cardiac myosin
• C Mycobacterial heat-shock protein 60 cross-reacting with joint cartilage
• D Epstein-Barr virus EBNA-1 protein cross-reacting with Ro/SSA

Explanation

In ankylosing spondylitis and other HLA-B27-associated spondyloarthropathies, the molecular mimicry hypothesis postulates that HLA-B27 presents arthritogenic peptides from gram-negative bacteria (Klebsiella pneumoniae in AS; Chlamydia trachomatis in reactive arthritis; Salmonella/Shigella in enteric reactive arthritis) that share sequence homology with HLA-B27 or self-peptides, triggering CD8+ T-cell responses that cross-react with self-antigens in the joint. Streptococcal M protein mimicry leads to rheumatic fever; EBV-Ro/SSA mimicry is in Sjögren syndrome.

Reference: Robbins & Cotran Pathologic Basis of Disease, 10th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

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