Jyoti Das, Ph.D.
Institute of Molecular Medicine,
254 Okhla Industrial Estate, Phase III
New Delhi: 110020, India
Phone: 011-41028710
Fax: 011-41028709
Email: Jyoti@immindia.org

Education:
M.Sc. Maharishi Dyanand University, Rohtak, Haryana.
Ph.D. Institute of Microbial Technolgy, Chandigarh.

Career History:
Feb 2009 - Present Senior Research Scientist; Institute of Molecular Medicine, New Delhi, India.
2002-2007 Adjunct Assistant Professor, Robert Wood Johnson Medical School, UMDNJ, NJ
2001-2002 Research Associate, Section of Immunobiology, Yale University
1999-2001 Post Doctoral training, Deptt. of Internal Medicine, Yale University

Awards and Honors:
Rapid Grant for Young Investigators by Department of Biotechnology (DBT), Ministry of Science and Technology, Govt. of India (2009).
Senior Research Fellowship from Council of Scientific and Industrial Research (CSIR), Government of India.
Junior Research Fellowship from Council of Scientific and Industrial Research (CSIR), Government of India.

Research Interest:
Transforming Growth Factor-b Is Dispensable for the Molecular Orchestration of Th17 Cell Differentiation.
IL-17-producing helper T cells (Th17) play a critical role in the pathophysiology of several autoimmune disorders. The differentiation of Th17 cells requires the simultaneous presence of an unusual combination of cytokines: IL-6, a pro-inflammatory cytokine, and TGF-β, an anti-inflammatory cytokine. However, the molecular mechanisms by which TGF-β exerts its effects on Th17 differentiation remain elusive. We observed that TGF- b promotes the differentiation of Th17 cells not by acting directly on the molecular orchestration in these cells, but rather by inhibiting the development of Th1 and Th2 cells.  These findings are consistent with a recent study providing evidence that TGF- b is not essential for the differentiation of IL-17-producing human helper T cells (Acosta-Rodriguez et al., 2007). In our studies, we showed that helper T cells that lack the differentiation machinery for both Th1 and Th2 cells (Stat-/-T-bet-/-) do not require TGF- b for Th17 cell differentiation.  In fact, impairment of Th1 and Th2 cells in BALB/c mice allowed the differentiation of encephalitogenic Th17 cells and susceptibility to EAE.  Although TGF-b was dispensable for Th17 differentiation in the absence of Th1 and Th2 responses, IL-6 was still required. To substantiate these data, we intend to generate Stat-/-T-bet-/- mice in TGF-bRII Dominant Negative (TGF-bRIIDN) background. CD4+ T cells from TGF-bRIIDN Stat-6-/-T-bet-/- mice will be subjected for the differentiation of Th17 and other T cell subsets. We will also generate Stat-6-/-T-bet-/- RoRgt-eGFP reporter mice. These mice will be useful for directly visualizing Th17 cells in vivo. Once the mechanism of differentiation of Th17 cells is cleared, we will be able to find molecular target for altering Th17 differentiation, and thereby the treatment of autoimmune inflammations.  

Molecular mechanism of susceptibility and resistance in allergic airway inflammations. 
In spite of the exposure to the same environment, some individuals develop allergic airway inflammations (AAI), whereas others are persistently resistant to AAI. Therefore, genetical differences play a critical role in determining the susceptibility in AAI. Similarly, in inbred strains of mice some strains are susceptible, whereas some other strains of mice are resistant. Recently, we have shown that Balb/C mice are susceptible whereas C3H mice are resistant to AAI. We also show that there was no difference in the differentiation of Th cells in these strains of mice. However, we noticed that C3H mice do not support the survival of Th2 cells in vivo. Our preliminary data indicated that Th2 cells derived from C3H mice are resistant to PGE2 mediated inhibition of apoptosis. Currently, we are working on deciphering the mechanisms of differential deaths of Th2 cells and thereby the AAI susceptibility in these strains of mice.                

Selected Publications:
Das, J., G. Ren, L. K. Kaer, F. Y. Shi and G. Das. 2009. TGF-b is dispensable in the differentiation, but selectively inhibits differentiation of Th1 and Th2 that promotes enrichment of Th17 cells. J. Exp. Med. (in press).

Das, J.,  P. Eynott, L. Van Kaer, R. Jupp, Y. F. Shi and G. Das. 2006. NKT cells and CD8+ T-cells are dispensable in a CD4+ T-cell dependent model of allergic airways inflammation. Nature Medicine. 12:1345-46.

Das, G.,  J. Das, P. Eynott, Y. Shi. 2006. Pivotal Roles of Major Histocompatibility Complex class Ib Restricted CD8+ T Cells in Autoimmune Diseases. J. Exp. Med. 203:2603-2611.

Das, J., S. Devdas, C. Liu, A. I. Roberts, G. Das and Y. F. Shi. 2006. Granzyme B Regulates Allergic Airway Inflammation by Inhibiting Activation Induced Cell Death of T helper 2 cells. Immunity: 25; 237-247.

Das, J., CH. Chan, Y.Yang, L. Cohn and A. Ray. 2001. A critical role for NF-kappa B in GATA3 expression and TH2 differentiation in allergic airway inflammation. Nature Immunol. 2:45-50.

Das, G.,  M. M. Augustine, J. Das, K. Bottomly and A. Ray. 2003. A regulatory role for CD4+CD8aa+ T cells in the intestinal epithelial layer in the prevention of colitis. Proc. Natal. Acad. Sci. USA. 100:5324-9.

Das J and Shi. Yufang. 2009. Prostaglanndin E2 mediated inhibition of activation induced cell death in T helper 2 cells determines susceptibility towards allergic airway Inflammation: (In preparation).

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