Bio

Professional Education


  • Doctor of Philosophy, Indian Institute of Science (2011)
  • Master of Science, Indian Institute of Technology, Bombay (2004)
  • Bachelor of Science, University of Pune (2003)

Stanford Advisors


Publications

Journal Articles


  • ATP release and autocrine signaling through P2X4 receptors regulate γδ T cell activation. Journal of Leukocyte Biology Manohar, M., Hirsh, M. I., Chem, Y., Woehrle, T., Karande, A. A., Junger, W. G. 2012; 92 (4): 787-794
  • Hypertonic stress regulates T cell function via pannexin-1 hemichannels and P2X receptors JOURNAL OF LEUKOCYTE BIOLOGY Woehrle, T., Yip, L., Manohar, M., Sumi, Y., Yao, Y., Chen, Y., Junger, W. G. 2010; 88 (6): 1181-1189

    Abstract

    Hypertonic saline (HS) resuscitation increases T cell function and inhibits posttraumatic T cell anergy, which can reduce immunosuppression and sepsis in trauma patients. We have previously shown that HS induces the release of cellular ATP and enhances T cell function. However, the mechanism by which HS induces ATP release and the subsequent regulation of T cell function by ATP remain poorly understood. In the present study, we show that inhibition of the gap junction hemichannel pannexin-1 (Panx1) blocks ATP release in response to HS, and HS exposure triggers significant changes in the expression of all P2X-type ATP receptors in Jurkat T cells. Blocking or silencing of Panx1 or of P2X1, P2X4, or P2X7 receptors blunts HS-induced p38 MAPK activation and the stimulatory effects of HS on TCR/CD28-induced IL-2 gene transcription. Moreover, treatment with HS or agonists of P2X receptors overcomes T cell suppression induced by the anti-inflammatory cytokine IL-10. These findings indicate that Panx1 hemichannels facilitate ATP release in response to hypertonic stress and that P2X1, P2X4, and P2X7 receptor activation enhances T cell function. We conclude that HS and P2 receptor agonists promote T cell function and thus, could be used to improve T cell function in trauma patients.

    View details for DOI 10.1189/jlb.0410211

    View details for Web of Science ID 000285867500016

    View details for PubMedID 20884646

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