| Summary: | 博士 === 國防醫學院 === 生命科學研究所 === 102 === Retinoic acid (RA), an active metabolite converted from vitamin A, plays an active role in immune function, such as defending against infections and immune regulation. Although RA affects various types of immune cells, including antigen-presenting cells, B lymphocytes, and T lymphocytes, whether it affects natural killer T (NKT) cells remain unknown. In this study, we found that RA decreased interferon (IFN)-gamma production by activated NKT cells through T cell receptor (TCR) and CD28. In addition to reduce NKT cells activation, we also found that RA reduced extracellular signal-regulated kinase (ERK) phosphorylation, but increased phosphatase 2A (PP2A) activity in TCR/CD28-stimulated NKT cells. The increased PP2A activity at least partly contributed to the reduction of ERK phosphorylation. As inhibition of ERK activation decreased IFN-gamma production by TCR/CD28-stimulated NKT cells, RA may down-regulated IFN- production by TCR/CD28-stimulated NKT cells through the PP2A-ERK pathway. Our results demonstrated a novel function of RA in modulating the IFN-gamma expression by activated NKT cells.
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