Toxic shock syndrome toxin-1 (TSST-1) of Staphylococcus aureus acts as a superantigen. Its mechanism of T cell activation differs from conventional antigen presentation in that it:
- A Requires processing by antigen-presenting cells and MHC class II presentation
- B Activates T cells through toll-like receptor 2 signalling on macrophages
- C Binds simultaneously to MHC class II and Vβ region of TCR outside the antigen-binding groove, activating up to 20% of T cells ✓
- D Binds to MHC class I and activates CD8+ cytotoxic T cells exclusively
Explanation
Superantigens such as TSST-1 bypass conventional antigen processing; they bind non-specifically to the lateral face of MHC class II molecules (outside the peptide-binding groove) and to the variable beta (Vβ) region of TCR simultaneously. This cross-linking activates a large proportion (5–20%) of all T cells bearing the relevant Vβ segment, leading to massive cytokine release (TNF-α, IL-1, IL-2, IFN-γ) — the cytokine storm underlying TSS. Conventional antigens activate <0.01% of T cells after APC processing and MHC groove presentation.
Reference: Ananthanarayan & Paniker's Textbook of Microbiology, 11th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.