Staphylococcus aureus TSST-1 causes toxic shock syndrome through a superantigen mechanism. This differs from conventional antigen presentation because TSST-1:
- A Is processed and presented in MHC class I groove to CD8+ T cells
- B Binds MHC class II outside the antigen-binding groove and activates Vβ-specific T cells ✓
- C Activates B cells independently via toll-like receptor 2
- D Crosslinks IgE on mast cells causing immediate hypersensitivity
Explanation
Superantigens like TSST-1 and staphylococcal exotoxins bind outside the polymorphic peptide-binding groove of MHC class II, simultaneously engaging the Vβ region of TCR; this activates up to 20-30% of all T cells (vs <0.01% in conventional activation), causing a cytokine storm (TNF, IL-1, IL-6). Conventional antigens are processed and presented in the MHC groove. TSST-1 acts on T cells via TCR/MHC class II, not B cells via TLR2. Crosslinking IgE is the mechanism of type I hypersensitivity allergens.
Reference: Ananthanarayan & Paniker's Textbook of Microbiology, 11th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.