This evening dinner update, in collaboration with the Erie Department of Health and Erie HIV Task Force, will be held at the Bayfront Convention Center. The presenters will discuss Sexual Health History Taking and Sexual Health and Stigma, followed by a panel of local providers.
Abstract: Tim-3 is highly expressed on a subset of T cells during T cell exhaustion, in settings of chronic viral infection and tumors. Using LCMV Clone 13, a model for chronic infection, we have found that Tim-3 is neither necessary nor sufficient for the development of T cell exhaustion. Nonetheless, expression of Tim-3 was sufficient to drive resistance to PD-L1 blockade therapy during chronic infection. Strikingly, expression of Tim-3 promoted development of short-term effector T cells, at the expense of memory precursor development, after acute LCMV infection. These effects were accompanied by increased Akt/mTOR signaling in T cells expressing endogenous or ectopic Tim-3. Conversely, Akt/mTOR signaling was reduced in effector T cells from Tim-3 deficient mice. Thus, Tim-3 is essential for optimal effector T cell responses, but may also contribute to exhaustion, by restricting development of long-lived memory T cells. Taken together, our results suggest that Tim-3 is actually more similar to co-stimulatory receptors that are upregulated after T cell activation, rather than a dominant inhibitory protein like PD-1. These findings have significant implications for the development of anti-Tim-3 antibodies as therapeutic agents.
Mentor: Lawrence Kane, PhD (Mentor)
Advisor: Charles Rinaldo, PhD (Chair)
Last Updated On Friday, March 30, 2018 by Abby Kincaid
Created On Wednesday, March 07, 2018