Presentation Type
Poster
Regulation of Interleukin-10 by HDACs on Mantle Cell Lymphoma
Abstract
Mantle Cell Lymphoma still remains one of the aggressive and incurable B cell malignancies. New approaches to treat MCL are being proposed, including epigenetic regulation as a way to alter gene expression, which could subsequently induce immune priming over immune tolerance. Histone deacetylases are key players in the regulation of a wide variety of genes and could have a central role in anergy. IL-10 is a primary cytokine in the inhibition of the immune response; its effect must be overcome in order to achieve a better immune response. We studied the expression of IL-10 in B cell lines as a model of Antigen Presenting Cells after treatment with the pan-inhibitor Trichostatin A and the HDAC 6 specific inhibitor Compound 7, in order to elucidate the role of HDACs in the regulation of IL-10, and thus the consequent implications in the inhibition of the immune response. We found that HDACs inhibitors abrogate the Lypopolysaccharide mediated up-regulation of IL-10 in B cells. Also HDAC6 inhibition considerably diminished IL-10 expression in B cells pointing to a positive correlation between HDAC 6 and IL-10. These preliminary findings point to HDAC6 as a primary player in the improvement of the immune response.
Categories
Biomedical Sciences
Research Type
Research Assistant
Mentor Information
Dr. Eva Sahakian
Regulation of Interleukin-10 by HDACs on Mantle Cell Lymphoma
Mantle Cell Lymphoma still remains one of the aggressive and incurable B cell malignancies. New approaches to treat MCL are being proposed, including epigenetic regulation as a way to alter gene expression, which could subsequently induce immune priming over immune tolerance. Histone deacetylases are key players in the regulation of a wide variety of genes and could have a central role in anergy. IL-10 is a primary cytokine in the inhibition of the immune response; its effect must be overcome in order to achieve a better immune response. We studied the expression of IL-10 in B cell lines as a model of Antigen Presenting Cells after treatment with the pan-inhibitor Trichostatin A and the HDAC 6 specific inhibitor Compound 7, in order to elucidate the role of HDACs in the regulation of IL-10, and thus the consequent implications in the inhibition of the immune response. We found that HDACs inhibitors abrogate the Lypopolysaccharide mediated up-regulation of IL-10 in B cells. Also HDAC6 inhibition considerably diminished IL-10 expression in B cells pointing to a positive correlation between HDAC 6 and IL-10. These preliminary findings point to HDAC6 as a primary player in the improvement of the immune response.
