Alan Sher, Ph.D.Building 50, Room 614050 South DriveBethesda, MD 20892-8003Phone: 301-496-3535 Fax: firstname.lastname@example.org
Chief, Laboratory of Parasitic Diseases
Chief, 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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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.
Jankovic D, Kullberg MC, Feng CG, Goldszmid RS, Collazo CM, Wilson M, Wynn TA, Kamanaka M, Flavell RA, Sher A. Conventional T-bet+Foxp3(-)Th1 cells are the major source of host-protective regulatory IL-10 during intracellular protozoan infection. J Exp Med. 2007 Feb 19;204(2):273-83.
Yarovinsky F, Zhang D, Andersen JF, Bannenberg GL, Serhan CN, Hayden MS, Hieny S, Sutterwala FS, Flavell RA, Ghosh S, Sher A. TLR11 activation of dendritic cells by a protozoan profilin-like protein. Science. 2005 Jun 10;308(5728):1626-9.
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Last Updated February 11, 2013