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
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 adaptive immune system has an evolutionary mandate to protect the integrity of the host – predominantly by fighting off infectious agents and malignancies. Nevertheless the machinery it uses to protect the host also has the potential to injure the body and cause debilitating autoimmune diseases. Understanding the regulatory networks that have evolved to maintain optimal protective immunity with minimal damage to the host is the focus of the Nevil lab. We employ mouse model systems to examine basic cellular and molecular questions in T cell Immunology.
For more details and up to date information about current projects, please visit our Laboratory pages at http://nevillab.org