Professor of Medicine and Immunology
Dr. Prabir Ray received his Ph.D. from Calcutta University in India. He received postdoctoral training at Cornell University, Ithaca, NY and at Sloan-Kettering Cancer Institute in New York. He was on the faculty at Yale University between 1990 and 2001 after which he joined the faculty in Pulmonary, Allergy and Critical Care Medicine with a co-appointment in the Department of Immunology at the University of Pittsburgh. Prabir Ray received his Ph.D. from Calcutta University in India. He received postdoctoral training at Cornell University, Ithaca, NY and at Sloan-Kettering Cancer Institute in New York. He was on the faculty at Yale University between 1990 and 2001 after which he joined the faculty in Pulmonary, Allergy and Critical Care Medicine with a co-appointment in the Department of Immunology at the University of Pittsburgh.
Dr. Ray’s research interest lies in the immunoregulatory mechanisms of lung inflammation as they relate to disease inception and resolution. Dr. Ray pioneered the development of inducible cell-specific transgenic mice in the early years of his career at Yale University and using this system showed an important role for the growth factor KGF in protection from lung epithelial cell death during lung injury. His research in the area of innate immune mechanisms regulating adaptive immunity led to the identification of a central role of the c-kit-PI3 kinase axis in promoting IL-6 but inhibiting IL-12 production in dendritic cells resulting in Th17 and Th2 differentiation and development of the asthma phenotype in an animal model. This work was chosen for the Year in Immunology 2010 publication of the New York Academy of Sciences.
Ongoing research in Dr. Ray’s laboratory encompasses two major areas, which are studies of innate immune mechanisms that mediate resolution of lung inflammation and protect from lung injury after pneumonia and the impact of early life viral infections on immunoregulatory mechanisms in the lung. In collaborative studies between his lab and that of Dr. Anuradha Ray, for the first time a pathogen, respiratory syncytial virus, was shown to disable Tregs in early life thereby compromising immune tolerance and increasing the risk for asthma in later life. He is particularly interested in differences in host defense mechanisms between newborns and older adults that causes increased susceptibility to respiratory viruses in early rather than in later life. His work has also for the first time identified the development of myeloid-derived suppressor cells (MDSCs) in the lung in response to bacterial infection and concomitant TLR/MyD88 signaling that play an important role in resolution of bacterial pneumonia. These studies utilize animal models of disease and human samples which are analyzed using immunological, molecular, biochemical and imaging techniques. Dr. Ray’s research has been continuously funded by grants from the American Lung Association and the NIH.
Poe, S.L., Arora, M., Oriss, T.B., Yarlagadda, M., Isse, K., Khare, A., Levy, D.E., Lee, J.S., Mallampalli, R.K., Ray, A*., Ray, P*. (2013) STAT1-regulated Lung MDSC-like Cells Produce IL-10 and Efferocytose Apoptotic Neutrophils With Relevance In Resolution of Bacterial Pneumonia. Mucosal Immunol. (*-co-senior authors) 6:189-199.
Krishnamoorthy, N., Khare, A.*, Oriss, T.B.*, Raundhal, M., Morse, C., Yarlagadda, M., Wenzel, S.E., Moore, M.L., Peebles, Jr., R.S., Ray, A., Ray, P., (2012) Early infection with respiratory syncytial virus impairs regulatory T cell function and increases susceptibility to allergic asthma Nature Med. (*equal contribution; co-senior authors) 18:1525-1530. Faculty of 1000 Biology Evaluation-Must Read (8). First study to show that a pathogen can target Tregs to impair immune tolerance.
Arora, M., Poe, S.L., Oriss, T.B., Krishnamoorthy, N., Yarlagadda, M., Wenzel, S.E., Billiar, T.R., Ray, A., Ray, P. (2010) TLR4/MyD88-Induced CD11b+Gr-1intF4/80+ Non-Migratory Myeloid Cells Suppress Th2 Effector Function in the Lung. Mucosal Immunol. 3:578-593.Faculty of 1000 Biology Evaluation Must Read (8).
Ray, P., Krishnamoorthy, N., Oriss, T.B., Ray, A. (2010) Signaling of c-kit in dendritic cells influences adaptive immunity in Rose, N. (ed.) “Year in Immunology 2010” Annals New York Acad. Sci. 1183:104-122.
Krishnamoorthy, N., Oriss, T.B., Paglia, M., Fei, M., Vanhaesebroeck, B., Ray, A. and Ray, P. (2008) Activation of c-Kit in dendritic cells regulates T helper cell differentiation and allergic asthma. Nature Medicine 14:565-573.
Chen, Li, Arora, M., Yarlagadda, M., Oriss, T., Krishnamoorthy, N., Ray, A., Ray, P., (2006) Distinct Responses of Lung and Spleen Dendritic Cells to the TLR9 Agonist CpG Oligodeoxynucleotide1. J. Immunol. 177: 2373-2383
Arora, M., Chen, L., Paglia, M., Gallagher, I., Allen, J.E., Vyas, Y.M., Ray, A., Ray, P., (2006) Simvastatin Promotes Th2-type Responses Through the Induction of Chitinase Family Member Ym1in Dendritic Cells. Proc. Natl. Acad. Sci. USA, 103:7777-7782.
Lu, Y., Pan, Z.Z., Devaux, Y., Ray P. (2003) PAK4 interacts with the keratinocyte growth factor receptor and participates in KGF-mediated inhibition of oxidant-induced cell death. J. Biol. Chem. 278:10374-10380
Ray, P., Devaux, Y., Stolz D.B., Yarlagadda, M., Watkins S.C, Liu, W., Lu, Y., Yang, X.F., Ray, A. (2003) Inducible expression of keratinocyte growth factor (KGF) in mice inhibits lung epithelial cell death induced by hyperoxia. Proc. Natl. Acad. Sci. USA, 100:6098-6103.
Lu, Y.B., Parkyn, L., Liu, W. Otterbein, L., Yang, L., Kureishi, Y., Walsh, K., Ray, P. (2001). Activated Akt protects the lung from oxidant-induced injury and delays death of mice. J. Exp. Med. 193: 545-549.
Yang. L., Cohn, L., Zhang, D. -H., Homer, R., Ray, A., Ray, P. (1998) Essential role of nuclear factor kappa beta in the induction of eosinophilia in allergic airway inflammation J. Exp. Med. 188: 1739-1750
Dr. Ray is featured in many articles, including those below: