Superantigen exposure causes uncoordinated release of cytokines from which cells?

Superantigen exposure causes uncoordinated release of cytokines from which cells?

• A. IFN-γ from Th1 cells and IL-1, IL-6, TNF-α from macrophages
• B. IL-2 and IL-4
• C. IL-10 and TGF-β
• D. IL-17 and IL-22

Answer: (A)

Superantigens trigger a massive, nonspecific activation of T cells by cross-linking the T-cell receptor to MHC class II on antigen-presenting cells, bypassing normal antigen recognition. This rapid, polyclonal T-cell activation leads to a surge of cytokines from two main sources: T cells release IFN-γ (a hallmark Th1 cytokine), which strongly activates macrophages; and macrophages release IL-1, IL-6, and TNF-α, driving fever, inflammation, and vascular instability. The combined action of these cytokines produces the systemic inflammatory response seen with toxic shock syndrome. Other cytokine profiles don’t fit the pattern: IL-2 and IL-4 are more about T-cell growth and differentiation rather than the broad cytokine storm; IL-10 and TGF-β are regulatory/anti-inflammatory; IL-17 and IL-22 are linked to mucosal immunity and neutrophil recruitment rather than the classic T-cell plus macrophage cytokine surge.

Superantigens trigger a massive, nonspecific activation of T cells by cross-linking the T-cell receptor to MHC class II on antigen-presenting cells, bypassing normal antigen recognition. This rapid, polyclonal T-cell activation leads to a surge of cytokines from two main sources: T cells release IFN-γ (a hallmark Th1 cytokine), which strongly activates macrophages; and macrophages release IL-1, IL-6, and TNF-α, driving fever, inflammation, and vascular instability. The combined action of these cytokines produces the systemic inflammatory response seen with toxic shock syndrome.

Other cytokine profiles don’t fit the pattern: IL-2 and IL-4 are more about T-cell growth and differentiation rather than the broad cytokine storm; IL-10 and TGF-β are regulatory/anti-inflammatory; IL-17 and IL-22 are linked to mucosal immunity and neutrophil recruitment rather than the classic T-cell plus macrophage cytokine surge.