Regulation of CD8 T cell effector function by NFKBID 9358

Abstract Description Chronic antigen exposure imposes a state of hypo-responsiveness called T cell exhaustion. Exhaustion is characterized as enhanced expression of inhibitory receptors, decreased expression of cytokines, decreased proliferation as well as decreased cytotoxicity. Cancers further exacerbate inadequate anti-tumor immunity by fostering a metabolically hostile microenvironment which hampers T cell survival. My research in the Hogan lab is focused on arming T cells to mount effective anti-tumor responses by overcoming exhaustion, and increasing T cell numbers in the face of rapidly growing tumors by enhancing T cell proliferation and survival. I have demonstrated that overexpression of the 50kD isoform of NFKBID, an IkB factor that regulates NF-κB transcriptional activity, enhances T cell expansion and short-lived effector functions in melanoma, reducing the rate of tumor growth, and extending the survival of tumor bearing mice. Topic Categories Tumor Immunology: Cellular Responses and Tumor Microevironment (TIME)