W. Henry Boom, M.D.
Professor of Medicine
Vice Chair for Research, Department of Medicine
Director, Tuberculosis Research Unit
Education
M.D. University of Rochester, 1979
Infectious Disease Fellowship, Massachusetts General Hospital,
Harvard School of Public Health and Brigham and Women’s
Hospital, 1983 -1988
Internal Medicine Residency and Chief Residency, George Washington
University Medical Center, 1979-1983
Office 216-368-4844
Email whb@case.edu
Research Area
Tuberculosis
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
