, Volume 28, Issue 5, pp 558-570
Date: 08 May 2008

15-Deoxy-Δ12,14 -Prostaglandin J2 and Curcumin Modulate the Expression of Toll-like Receptors 4 and 9 in Autoimmune T Lymphocyte

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Experimental allergic encephalomyelitis (EAE) is a T cell-mediated autoimmune disease model for multiple sclerosis (MS). We have shown earlier that 15-deoxy-Δ12,14-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.


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.


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.