Introduction  

Experimental allergic encephalomyelitis (EAE) is a T cell-mediated autoimmune disease model for multiple sclerosis (MS). We have shown earlier that 15-deoxy-Δ^12,14-prostaglandin J₂ (15d-PGJ₂) and curcumin ameliorate EAE by modulating inflammatory signaling pathways in T lymphocytes. Toll-like receptors (TLRs), expressed primarily in innate immune cells, play critical roles in the pathogenesis of EAE. T lymphocytes also express TLRs and function as costimulatory receptors to upregulate proliferation and cytokine production in response to specific agonists.

Discussion  

In this study, we show that naïve CD4⁺ and CD8⁺ T cells express detectable levels of TLR4 and TLR9 and that increase after the induction of EAE in SJL/J and C57BL/6 mice by immunization with PLPp139–151 and MOGp35–55 antigen, respectively. It is interesting to note that in vivo treatment with 15d-PGJ2 or curcumin results in a significant decrease in TLR4 and TLR9 expression in CD4⁺ and CD8⁺ T cells in association with the amelioration of EAE.

Conclusion  

Although the exact mechanisms are not known, the modulation of TLR expression in T lymphocytes by 15d-PGJ₂ and curcumin suggests new therapeutic targets in the treatment of T cell-mediated autoimmune diseases.