Microbiology and Immunology
Member, Marlene and Stewart Greenebaum Comprehensive Cancer Center
Education and Training
Nevil Singh is a graduate of the Tata Institute of Fundamental Research (TIFR, Bombay, India) where his thesis work focused on vaccine-antigens against the malarial parasite, Plasmodium falciparum. He then joined Ron Schwartz’s group at the NIAID, NIH for a post-doctoral fellowship, examining T cell tolerance to self-proteins. Subsequently, as a Research Scientist at the NIAID, he studied the mechanisms controlling the responsiveness and frequency of helper T cells. He joined the faculty of UMDSOM in 2013.
T cell activation & differentiation, Immunological tolerance, Immunological Memory, Neuroimmunology, Adaptive immunity to infections, Dendritic cell activation, IL-12 family cytokines, Tumor Immunology, Cancer Immunology
Selected recent publications:
Singh, N. J., Bando, J.K. and Schwartz, R.H. (2012) Subsets of non-clonal neighboring CD4+ T cells specifically regulate the frequency of individual antigen-reactive T cells (Immunity. 2012 Oct 19;37(4):735-46., - featured on the cover of October 2012). PubMed
Steinert, E., Schwartz, R.H., and Singh, N. J.(2012) At low precursor frequencies the helper T cell response to chronic self-antigen presentation in vivo, is followed by anergy without deletion. (Eur J Immunol. 2012 Nov; 42(11): 2875-80) PubMed
Oh, S., Schwartz, R.H., and Singh, N. J. (2012) Development and tolerization of hyperacute rejection in a transgenic GVH model. (Transplantation. 2012 Aug 15;94(3):234-40) PubMed
Abdi, K., Singh, N. J. and Matzinger, P. (2012), Lipopolysaccharide-Activated Dendritic Cells: "Exhausted" or Alert and Waiting?. (J Immunol.2012 Jun 15;188(12):5981-9) PubMed
Quiel, J., Caucheteux, S., Laurence, A., Singh, N. J., Bocharov, G., Ben-Sasson, S. Z., Grossman, Z. and Paul, W. E. (2011), Antigen-stimulated CD4 T-cell expansion is inversely and log-linearly related to precursor number. (Proc Natl Acad Sci U S A. 2011 Feb 22;108(8):3312-7) PubMed
The Nevil Lab is interested in understanding the basic biology of T cells - focusing on how CD4 T cells respond to pathogens, tumors and self-antigens. The overall outcome of a T cell response depends on multiple signals which impinge on individual T cells. The predominant one involves signals from the antigen, which are sensed by the T cell receptor (TCR). Projects in the lab examine how shorter duration of TCR signals (like those coming from acute infections, vaccines etc.) drives the productive activation of T cells while those arising from persistent antigens (e.g. tumors, chronic viral infections, self-antigens) tends be rather ineffective at sustaining a T cell response. Understanding this dichotomy is critical to improving immunity to tumors (and is the basis of therapeutic approaches such as checkpoint blockade). In addition, T cell functions are also modified by signals from the innate immune system, stromal cells and even the nervous system. We examine each of these using a variety of mouse model systems.
For more details and up to date information about current projects, please visit our Laboratory pages at http://nevillab.org