Superantigens induce IL-17 production from polarized Th1 clones

• Superantigens stimulate IL-17 production by well differentiated cloned Th1 cells.
• Superantigen-induced IL-17 production is partially MHC II and TCR dependent.
• Superantigen-induced IL-17 production may be involved in exacerbation of autoimmune diseases associated with infections.

Differentiation of naïve CD4+ T cells has been considered to be an irreversible event and, in particular, the plasticity is believed to be completely lost in Th1 subset in vitro after multiple stimulations. However, here we demonstrate that highly polarized myelin oligodendrocyte glycoprotein (MOG)- and herpes simples virus-specific Th1 clones were still capable of producing IL-17 upon superantigen stimulation. Anti-MHC class-II and anti-TCR αβ chains partially blocked superantigen-induced IL-17 production. These findings suggest that fully differentiated Th1 cells still have capability to produce cytokines of other Th subsets and production of IL-17 by MOG-specific Th1 cells may have implication in initiation and/or exacerbation of neurological autoimmune diseases.