Office Address(es):
UPMC Montefiore Hospital - NW628
3459 Fifth Avenue
Pittsburgh, PA 15213
Phone: 412-692-2118
Fax: 412-692-2260

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. 

Academic and Research Interests:

Research in Dr. Ray’s laboratory is focused on the following two major areas:

1) Effect of immunomodulatory agents (pathogens, drugs) on dendritic cell function influencing immune responses in the lung. Dendritic cells (DCs) and epithelial cells exist in close apposition in the lung.  Drug therapy, allergen exposure or infection can alter the cytokine-chemokine milieu in the tissue.  This altered microenvironment can influence DC function directly or indirectly via effects on epithelial cells or other cells of the innate immune system. Dr. Ray’s research has shown that statin, a cholesterol-lowering agent, can influence DC character and this statin-exposed DC induces a Th2 bias in the immune response (PNAS 103:7777, 2006).  More recently, they have discovered that dual upregulation of the receptor tyrosine kinase, c-kit, and its ligand, stem cell factor (SCF), on DCs promotes Th2 and Th17 differentiation (Nature Medicine 14:565, 2008).  This study highlights an important, previously unrecognized, role of c-kit in immunoregulation.  Another focus of his ongoing studies is to understand mechanisms by which cells of the innate immune system influence adaptive immune responses in the lung using models of lung infection and allergic asthma.

2) Mechanisms by which growth factors protect the lung from acute lung injury and fibrosis. Because of its location and function, the lung is vulnerable to a variety of insults. Insults to the lung cause injury and abnormal repair of the injury can result in fibrosis, which inhibits normal lung function. Dr. Ray’s research has shown that some growth factors like keratinocyte growth factor (KGF), whose activity is largely restricted to epithelial cells, can protect the lung from injury and inhibit fibrosis.  Using inducible transgenic and knockout mice, yeast two-hybrid system, microarray approaches and imaging technology they have been addressing the molecular mechanisms downstream of these biological signals that cause inhibition of lung injury and fibrosis (JEM 193: 545, 2001; PNAS, 100:6098, 2003).  These studies show that specific signaling pathways induced in epithelial cells in the lung can protect the lung from a variety of insults including fibroproliferative responses. His current studies are directed towards understanding the role of epithelial cells in lung fibrosis and its prevention by specific growth factors.

Key Publications:

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