Author: Kristin Wallace

Dr. Kamal Khanna Receives UConn Health’s 2016 SPARK Grant

Dr. Kamal Khanna
Dr. Kamal Khanna is one of the recipients of UConn Health’s 2016 SPARK Grant Competition. These awards aim to help investigators move ideas into the earliest stages of commercialization and development. Dr. Khanna’s project is focused on determining the efficacy of novel vaccine technology developed by Carogen Corporation in preventing and treating Clostridium Difficile infections, which are the most commonly acquired infections in hospitals.

Key Publication in PNAS from the Laboratory of Dr. Kamal Khanna

Dr. Kamal Khanna
Dr. Kamal Khanna’s lab and research on T cell migration during a viral infection has earned a key publication in the Proceedings of the National Academy of Sciences (PNAS). This study lays the foundation for developing better therapeutic strategies against autoimmune and infectious diseases that target T cell intrinsic S1P-S1PR axis. 

The T cells have to get to the tissue where there is an infection in order to help eradicate the invading virus or bacteria.  Thus, the control of a microbial infection by effector T cells is intrinsically linked to their migration. However, little is known about the mechanisms that control effector T cell egress after infection. We need to understand this important biological process in order to develop better vaccines and immuno-therapeutic strategies to treat infectious diseases and cancers.  In the current study we investigated the role of an important protein called sphingosine-1-phosphate-receptor-1 (S1PR1) in regulating T cell migration during a viral infection.  S1PR is currently being targeted for therapy against several autoimmune diseases such as multiple sclerosis (MS). In our current study we used multi-photon microscopy to visualized in real time pathogen-specific, effector T cell migration in live animals within, and from, the draining lymph node (dLN).  We utilized a novel inducible mouse model with temporally disrupted S1PR1 gene specifically in endogenous effector T cells.  We demonstrate that S1PR1 signaling is the most critical mechanism that regulates effector T cell egress from the dLN following a local infection, and even in the absence of retention signals, T cell intrinsic S1PR1 signaling is the dominant mechanism that regulates transendothelial migration and effector T cell emigration from the dLN and thus, we conclude that S1PR1 is the master regulator of effector T cell egress after infection.  Thus, our study lays the foundation for developing better therapeutic strategies against autoimmune and infectious diseases that target T cell intrinsic S1P-S1PR axis.

For more information on this paper, please go to http://www.pnas.org/content/early/2016/02/08/1516485113.abstract