W. Henry Boom, MD
Professor of Medicine
Vice Chair for Research, Department of Medicine
Director, Tuberculosis Research Unit
Phone: (216) 368-4847
Fax: (216) 368-2034
E-mail: whb@case.edu
Education
MD- University of Rochester, 1979
Residency- Internal Medicine Residency and Chief Residency, George Washington University Medical Center, 1983
Fellowship- Massachusetts General Hospital
Harvard School of Public Health and Brigham and Women’s Hospital, 1988
Laboratory
Research
T cells play a critical role in the immune response to the intracellular pathogen M. tuberculosis, which is estimated to infect one third of the world's population. T cells regulate the acquired immune response which controls primary infection and provide protection against exogenous reinfection. CD4+ T cells traditionally have been considered the main T cell subset responsible for regulating protective immune responses to M. tuberculosis. However, in addition to the CD4+ T cell, both gamma-delta T cell receptor bearing T cells (gamma delta cells) and CD8+ T cells have a role in protective immunity to M. tuberculosis. The study of CD4+, CD8+ and gamma delta T cell responses to M. tuberculosis is the main interest of my laboratory.
The focus is on characterization of mycobacterial antigens recognized by CD4+ and gamma-delta T cells, the role of cytokines such as IL-2, IL-12, IFN-gamma, IL-10 and TGF-beta in modulating the T cell responses to M. tuberculosis, the functional interaction of antigen-specific T cells with macrophages infected with mycobacteria, and the mechanisms used by M. tuberculosis infected macrophages to process and present antigens from the phagosome to the cell surface to these different T cell subsets. Recent studies have focused on identifying molecules of M. tuberculosis that interfere with MHC-II antigen processing. Specifically the role of mycobacterial lipoproteins and TLR receptors in regulating MHC-II antigen processing has become a major focus.
These studies use cellular immunological and cell biologic approaches to study the biology of M. tuberculosis infected macrophages and T cells. In addition, a murine in vivo model of M. tuberculosis infection of the lung is used to study the unique micro-environment where M. tuberculosis infection occurs and immune responses are initiated.
Selected Publications
• Ramachandra L, Noss EN, Boom WH, Harding CV (2001) Processing of M. tuberculosis antigen 85B involves intra-phagosomal formation of peptide:MHC-II complexes and is inhibited by live bacilli that decrease phagosome maturation. J Exp Med 194, 1421-1432.
• Rojas RE, Torres M, Fournie JJ, Harding CV, Boom WH (2002) Phosphoantigen presentation by macrophages to M. tuberculosis – reactive Vgamma9Vdelta2 + T cells: modulation by Chloroquine. Infection and Immunity 70, 4019-4027.
• Pai RK, Askew D, Boom WH, Harding CV (2002) Regulation of Class II Major histocompatability complex expression in professional antigen presenting cells: role of types I, III, IV class II transactivator. J Immunology 169, 1326-1333.
• Canaday D, Beigi R, Silver RF, Harding CV, Boom WH*, Dubyak GR* (2002) ATP and control of intracellular growth of mycobacteria by T cells. Infection and Immunity 70, 6456-6459. *Joint Senior Authorship
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