Title: Faculty & research interests

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Steven L. Reiner
Steven L. Reiner, MD
Professor
Full Member

Department: Microbiology and Immunology

HHSC 912A
212-305-5177
sreiner@columbia.edu


Personal Website

Disease Models: Immune Disorders, Cancer

Stem Cell Categories: Adult stem cells, Cancer stem cells

Model Organisms: Human, Rodent

Themes: Blood, Cancer

When recruited into an immune response, a naive lymphocyte undergoes a program of rapid proliferation and many of its cellular progeny undergo terminal differentiation. Some antigen-specific daughter cells, however, remain as long-lived replicas of the useful lymphocyte, so-called memory cells. This property of self-renewal (stem-ness) forms the basis for successful vaccination. Using lymphocytes as a model system, we have provided evidence that asymmetric cell division may be a way for many mobile, non-polarized cells to generate cell fate diversity among their progeny. We are using static and time-lapsed imaging, genetic, and biochemical methods to better understand the nature and extent of asymmetric cell division in multi-celled beings. It is predicted that this will have immediate relevance for the way in which blood stem cells and metastatic cancer stem cells can generate diverse progeny despite their lack of obvious polarity. Studies of lymphocyte differentiation during the immune response should continue to become an increasingly useful model for inquiry into the fundamental problem of regulated gene expression in dividing, differentiating, and highly mobile cells.



Publications:

Gordon, S.M., J. Chaix, L.J. Rupp, J. Wu, S. Madera, J.C. Sun, T. Lindsten, and S.L. Reiner.
The transcription factors T-bet and Eomes control key checkpoints of natural killer cell maturation. Immunity 36:55-67. (2012)

Barnett, B.E., M.L. Ciocca, R. Goenka, L.G. Barnett, J. Wu, T.M. Laufer, J.K. Burkhardt, M.P. Cancro and S.L. Reiner.
Asymmetric B cell division in the germinal center reaction. Science 335:342-344. (2012)

Chang, J.T., M.L. Ciocca, I. Kinjyo, V.R. Palanivel, C.E. McClurkin, C.S. DeJong, E.C. Mooney, J.S. Kim, N.C. Steinel, J. Oliaro, C.Y. Yin, B.I. Florea, H.S. Overkleeft, L.J. Berg, S.M. Russell, G.A. Koretzky, M.S. Jordan and S.L. Reiner.
Asymmetric proteasome segregation as a mechanism for unequal partitioning of the transcription factor T-bet during T lymphocyte division. Immunity 34:492-504. (2011)

Intlekofer, A.M., A. Banerjee, N. Takemoto, S.M. Gordon, C.S. Dejong, H. Shin, C.A. Hunter, E.J. Wherry, T. Lindsten and S.L. Reiner.
Anomalous type 17 response to viral infection by CD8+ T cells lacking T-bet and eomesodermin. Science 321:408-411. (2008)

Chang, J.T., V.R. Palanivel, I. Kinjyo, F. Schambach, A.M. Intlekofer, A. Banerjee, S.A. Longworth, K.E. Vinup, P. Mrass, J. Oliaro, N. Killeen, J.S. Orange, S.M. Russell, W. Weninger and S.L. Reiner.
Asymmetric T lymphocyte division in the initiation of adaptive immune responses. Science 315:1687-1691. (2007)

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