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Shiv Pillai, MD, PhDProfessor of MedicineHarvard Medical School
Associate GeneticistCenter for Cancer Research
The Pillai laboratory asks questions about the biology of the immune system and human genetics. Some of these questions are: 1) Can we manipulate the immune system to treat cancer and to increase immunological memory? 2) Can we understand how genetics and the environment affect lymphoid clones to drive common diseases? and 3) Can this latter information be used to better understand and develop new therapies for chronic inﬂammatory human diseases such as arthritis, lupus and IgG4-related disease? Our discovery of the role of an enzyme called Btk in the activation of B cells has contributed to the generation of Btk inhibitors that are effective in B cell malignancies and in trials of autoimmunity. One of the pathways we are currently studying suggests new approaches for the treatment of autoimmune disorders. We have also found a novel way to strengthen immune responses and enhance helper T cell memory that provides hope for developing more effective personalized immune-system based treatments for cancer.
Shiv Pillai MD, PhDPrincipal Investigator
* PhD Candidate
A novel human T cell subset that drives ﬁbrosis (NIAID Autoimmune Center of Excellence at MGH)
In studies on the immunology of IgG4 related disease and scleroderma, performed in collaboration with John Stone in Rheumatology, we have identiﬁed an unusual, clonally expanded and potentially “ﬁbrogenic” human CD4+ effector T cell subset. The differentiation and protective role of these CD4+ CTLs in cancer and chronic viral infections is currently being investigated.
Studies on murine and human B cell development and activation
We are using a number of single cell transcriptomic, epigenetic and genetic approaches to examine the heterogeneity and development of murine and human B cells, as well as the molecular bases of the processes of T-B collaboration and germinal center formation.
DNA methylation, B cell self-renewal and chronic lymphocytic leukemia
We have long been interested in cell fate decisions in B cell development and in the development of self-renewing B cell subsets. The roles of DNMT3a in B-1a B cell self-renewal and of speciﬁc methylation events in chronic lymphocytic leukemia are being investigated.
Dock2 regulates T cell memory and T-B collaboration
We have identified Dock2 as a regulator of the strength of the immune response and the generation of CD8+ and CD4+ T cell memory. This gene also contributes the strength of the germinal center response. The inactivation of this gene leads to the clearance of intracellular pathogens and may enhance anti-tumor immunity.
View a list of publications by researchers at the Pillai Laboratory
Yuen G, Demissie E and Pillai S. (2016) B cells and Cancer: a love-hate relationship. Trends in Cancer. in press.
Mahajan, V.S., Demissie, E., Mattoo, H., Viswanadham, V., Varki, A., Morris, R., and Pillai, S. (2016). Striking Immune Phenotypes in Gene-Targeted Mice Are Driven by a Copy-Number Variant Originating from a Commercially Available C57BL/6 Strain. Cell. Rep 15, 1901-1909.
Mattoo, H., Mahajan, V.S., Maehara, T., Deshpande, V., Della-Torre, E., Wallace, Z.S., Kulikova, M., Drijvers, J.M., Daccache, J., Carruthers, M.N., et al. (2016). Clonal expansion of CD4+ cytotoxic T lymphocytes in patients with IgG4-related disease. J Allergy Clin Immunol. Epub ahead of print.
Mahajan, V.S., and Pillai, S. (2016). Sialic acids and autoimmune disease. Immunol. Rev 269, 145-161.
Kamisawa, T., Zen, Y., Pillai, S., and Stone, J.H. (2015). IgG4-related disease. Lancet. 385, 1460-1471.
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