Staphylococcal toxic shock syndrome (TSS) is mediated by TSST-1, which acts as a superantigen. The superantigen mechanism that causes the massive cytokine release involves:

• A Direct binding to the antigen-binding groove of MHC class I
• B Cross-linking MHC class II on APCs with a specific TCR Vβ region, bypassing normal antigen processing ✓
• C Stimulation of MHC class II-independent B-cell activation via CD21
• D Activation of NK cells through NKG2D ligands

Explanation

TSST-1 is a superantigen that simultaneously binds the lateral (non-peptide) surface of MHC class II molecules and the Vβ domain of the T-cell receptor, outside the conventional antigen-binding site. This cross-linking non-specifically activates all T cells bearing the specific Vβ chain (up to 20% of all T cells), causing massive IL-2, IFN-γ, TNF-α release and the systemic shock syndrome. Normal antigen presentation involves processed peptide in the MHC groove activating only 0.001–0.0001% of T cells. Superantigens do not activate via MHC class I or NK cells.

Reference: Ananthanarayan & Paniker's Textbook of Microbiology, 11th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.