Rapid histone deacetylation and transient HDAC association in the IL-2 promoter region of TSST-1-stimulated T cells |
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Authors: | Kametani Yoshie Wang Lili Koduka Kanta Sato Takehito Katano Ikumi Habu Sonoko |
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Institution: | Department of Immunology, Tokai University School of Medicine, Isehara-shi, Kanagawa 259-1193, Japan. |
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Abstract: | It remains unclear how superantigen induces unresponsiveness in stimulated T cells. We analyzed the chromatin status of the interleukin-2 (IL-2) promoter region in T cells stimulated with toxic shock syndrome toxin-1 (TSST-1) superantigen using T cell receptor-transgenic T cells responding to ovalbumin (OVA) and TSST-1. Compared to OVA stimulation, na?ve T cells cultured with TSST-1 showed lower IL-2 expression after transient enhancement. Coincidentally, the acetylated histone H3 (AcH3) level at the IL-2 promoter region was first enhanced, and then decreased, in TSST-1-stimulated T cells. At the reduction stage of AcH3, histone deacetylase-1 (HDAC1) was markedly associated with the IL-2 promoter region in a TSST-1-specific manner without HDAC1 over-expression. The enhancement of HDAC1 association and IL-2 suppression was prevented by pre-treatment with HDAC inhibitor, but not once the anergy status was established. These results suggest that recruitment of HDAC1 in the IL-2 promoter region at the early stimulation stage with TSST-1 plays a pivotal role in sAg-induced anergy. |
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Keywords: | Superantigen Anergy Chromatin remodeling Histone acetylation Histone deacetylase-1 |
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