Alan Sher, Ph.D.Building 50, Room 614050 South DriveBethesda, MD 20892-8003Phone: 301-496-3535 Fax: email@example.com
Chief, Laboratory of Parasitic DiseasesChief, Immunobiology Section, LPD
The Immunobiology Section studies host resistance and immune regulation in parasitic and other infections of global importance. The ultimate goal of this work is immunologic disease intervention in the form of vaccination or immunotherapy. At the same time, our research on the host response to infection has provided insights into the effector functions and regulatory mechanisms used by the vertebrate immune system and in the role of innate pathogen recognition in these processes. Much of the work of the section is focused on the immunologic analysis in murine models of diseases induced by parasitic and bacterial agents (e.g., Toxoplasma gondii, Mycobacterium spp.), although the group is also engaged in several major clinical collaborations. The lab also has a major interest in the regulation of Th1-dependent immunopathology in T. gondii and mycobacterial infections as well as tuberculosis-HIV co-infection.
Dr. Sher received his Ph.D. from the University of California, San Diego, and did his postdoctoral training in the Division of Parasitology at the National Institute for Medical Research in Mill Hill, London. In 1980, after several years as a research associate and then assistant professor in the department of pathology at Harvard Medical School, he joined NIAID as a section chief in the Laboratory of Parasitic Diseases. Sher became chief of LPD in 2003 and was promoted to NIH Distinguished Investigator in 2011.
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Mayer-Barber KD, Andrade BB; Oland SD, Amaral EP, Barber DL, Gonzales J, Derrick S, Ruiru S, Nathella Pavan K, Wang W, Xing Y, Guolong Z, Ying C, Subash B, Marta C, Andres SM, Via LE, Barry III CE, Sher A. Host-directed therapy of tuberculosis based on interleukin-1-type I interferon crosstalk. Nature. 2014. In press.
Kugler DG, Mittelstadt PR, Ashwell JD, Sher A, Jankovic D. CD4+ T cells are trigger and target of the glucocorticoid response that prevents lethal immunopathology in toxoplasma infection. J Exp Med. 2013 Sep 23;210(10):1919-27.
Goldszmid RS, Caspar P, Rivollier A, White S, Dzutsev A, Hieny S, Kelsall B, Trinchieri G, Sher A. NK cell-derived interferon-γ orchestrates cellular dynamics and the differentiation of monocytes into dendritic cells at the site of infection. J Immunol. 2012 Aug 1;189(3):1104-11.
Mayer-Barber KD, Andrade BB, Barber DL, Hieny S, Feng CG, Caspar P, Oland S, Gordon S, Sher A. Innate and adaptive interferons suppress IL-1α and IL-1β production by distinct pulmonary myeloid subsets during Mycobacterium tuberculosis infection. Immunity. 2011 Dec 23;35(6):1023-34.
Mayer-Barber KD, Barber DL, Shenderov K, White SD, Wilson MS, Cheever A, Kugler D, Hieny S, Caspar P, Nunez G, Schlueter D, Flavell RA, Sutterwala FS, Sher A. Caspase-1 independent IL-1β production is critical for host resistance to Mycobacterium tuberculosis and does not require TLR signaling in vivo. J Immunol. 2010 Apr 1;184(7):3326-30.
Goldszmid RS, Coppens I, Lev A, Caspar P, Mellman I, Sher A. Host ER-parasitophorous vacuole interaction provides a route of entry for antigen cross-presentation in Toxoplasma gondii-infected dendritic cells. J Exp Med. 2009 Feb 16;206(2):399-410.
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Last Updated February 11, 2013