Prabir Ray, Ph.D.

Prabir Ray, Ph.D.


Office: NW 628 MUH

Lab: NW 648 MUH

Ph: 412-802-3192

Fax: 412-692-2260


  • B.Sc. - Calucutta University
  • M.Sc. - Calcutta University
  • Ph.D. - Calcutta University
  • Postdoc - Cornell University
  • Postdoc - Memorial Sloan-Kettering Cancer Center

Academic Affiliation

  • UPMC Endowed Chair in Lung Immunology in Medicine
  • Professor, Department of Medicine
  • Professor, Department of Immunology

About Research

Dr. Ray’s research is focused on two general areas: 1) Protective mechanisms in the lung that prevent acute lung injury specifically during bacterial pneumonia, and 2) Immunoregulatory mechanisms in the neonatal lung that defend against infections. To study these processes, he has developed mouse models of lung injury and infection using tissue-specific inducible transgenic or knockout mice.  Collectively, his findings on the one hand have significantly advanced our understanding of mechanisms that protect the lung from oxidative injury and on the other, have revealed immune mechanisms regulating lung inflammation in response to allergens, pathogens and immunomodulatory drugs.

In studies of bacterial pneumonia, Dr. Ray’s lab has identified pathways that induce the development of myeloid cells resembling myeloid-derived suppressor cells (MDSCs) in the lung that play an important role in immune regulation.  These studies have unraveled an interesting dynamic in the course of bacterial pneumonia that elicits the generation of IL-10-producing MDSCs during the late phase of inflammation. These MDSCs efficiently efferocytose apoptotic neutrophils thereby facilitating resolution of lung inflammation to restore pulmonary immune homeostasis. However, in non-resolving pneumonia, which causes significant morbidity and mortality, high levels of oxidized phospholipids generated during pneumonia impair IL-10 production from the MDSCs impairing resolution of inflammation. Ongoing studies are devoted to deciphering the underlying mechanisms.

Studies in Dr. Ray’s laboratory are also investigating host immune responses to infection by respiratory syncytial virus (RSV) in neonates using genetically altered mice as well as human primary lung and nasal epithelial cells co-cultured with immune cells. RSV infects every child by 2 years of age and in some infants can cause severe bronchiolitis requiring hospitalization. Multiple epidemiological studies have shown that severe disease induced by RSV is a risk factor for asthma development in later life. Work from his laboratory has for the first time identified an underlying mechanism which is impairment of regulatory T cell (Treg) function by RSV that breaches maternally-transferred immune tolerance (Nature Medicine 18:1525, 2012). His major current research focus in this area is on interactions between cells of the innate immune system and epithelial cells in early life that protect from RSV-induced pathology. These studies have the potential to identify targets for improving defense against RSV since effective vaccines against this virus are currently unavailable. Dr. Ray has trained multiple students, fellows and postdocs. His current research program involves active collaborations with scientists nationally as well as internationally.

Selected Publications

Raundhal, M., Morse, M., Khare, A., Oriss, T.B., Milosevic, J., Trudeau, J., Huff, R., Pilewski, J., Holguin, F., Kolls, J. Wenzel, S.E., Ray, P. ¶,, Ray, A. ¶, (2015) High IFN-g and Low  SLPI Mark Severe Asthma In Humans and Mice. J. Clin. Invest. doi:10.1172/JCI80911. PMCID:PMC4563754. ¶,-co-senior authors.

Khare, A., Chakraborty, K., Raundhal, M., Ray, P, Ray, A. (2015) Dual Function of PPARg in CD11c+ Cells Ensures Immune Tolerance in the Airways. Cutting edge: J Immunol. 195:431-435. PMCID: PMC4490989.

Poe SL, Arora M, Oriss TB, Yarlagadda M, Isse K, Khare A, Levy DE, Lee JS, Mallampalli RK, 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. 6:189-199 (*-co-senior author). PMCID: PMC3505806.

Ray A, Chakraborty K, Ray P. (2013) Immunosuppressive MDSCs induced by TLR signaling during infection and role in resolution of inflammation. Front Cell Infect Microbiol.  3:52 PMCID: PMC3776133.

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. 18:1525-1530. PMCID: PMC3641779. *equal contribution; co-senior authors. Faculty of 1000 Biology Evaluation-Must Read (8). First study to show that a pathogen can target Tregs to impair immune tolerance.

Ray, A., Khare, A., Krishnamoorthy, N., Ray. P. (2012). GATA-3. In Encyclopedia of Signalling Molecules. S. Choi, ed. Springer Philadelphia. pp. 760-769.

Krishnamoorthy, N., Oriss, T.B., Paglia, M., Fei, M., Vanhaesebroeck, B., Ray, A. and Ray, P. (2008) Activation of the c-kit-PI3 kinase Axis Induces the Regulatory Cytokine Interleukin-6 in Dendritic cells Impacting Allergic Immune Responses In the Lung. Nature Med. 14: 565-573.

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 Ym1 in Dendritic Cells. Pro. Natl. Acad. Sci. USA 103:7777-7782.

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. Otterbein, L. E., Kureishi, Y., Walsh, K., Ray, A., Ray, P. (2001). Activated Akt protects the lung from oxidant-induced injury and increases survival of mice. J. Exp. Med. 193: 545-549.