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.
- 15-Deoxy-Δ12,14-Prostaglandin J2 and Curcumin Modulate the Expression of Toll-like Receptors 4 and 9 in Autoimmune T Lymphocyte
Journal of Clinical Immunology
Volume 28, Issue 5 , pp 558-570
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- Springer US
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- Autoimmune disease
- Th1 cell
- toll-like receptor
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- Author Affiliations
- 1. Neuroscience Research Laboratory, Methodist Research Institute at Clarian Health, 1800 North Capitol Avenue, Noyes Building E-504C, Indianapolis, IN, 46202, USA
- 2. Department of Medicine, Indiana University School of Medicine, Indianapolis, IN, USA