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Michael E. Lamm, M.D.Professor Emeritus, past Chair of PathologyMailing Address: fax: (216) 368-0494 email: Michael.Lamm@Case.edu |
Biography
Dr. Michael Lamm completed his undergraduate career at Amherst College, Massachusetts in 1954. He went on
to earn his M.D. from the University of Rochestor, New York in 1959 and his M.S. in Chemistry at Case in
1962. Dr. Lamm was an intern and Assistant Resident in Pathology at Case’s Institute of Pathology
and University Hospitals of Cleveland. He became Senior Assistant Surgeon and Surgeon (Research Associate)
for the Section on Physical Chemistry at the National Institute of Mental Health, Bethesda, from 1962
until 1964. The next four years were spent as an Assistant Professor of Pathology at New York University.
Dr. Lamm continued on as an Associate Professor and then Professor of Pathology at New York University
until 1981. During this time period, he spent a year each as Visiting Scientist and Professor at the
University of Oxford’s Department of Biochemistry (R.R. Porter) and University of Geneva’s Department
of Pathology (P. Vassalli). From 1981 until 2001, Dr. Lamm served as Chair for Case’s Department of
Pathology. Presently, he is a Professor of Pathology at Case.
Research
Most infections occur along the mucosal lining of the respiratory and gastrointestinal tracts, or result
from penetration of these sites by pathogenic microorganisms. For some time it has been recognized that
IgA antibodies in the mucosal secretions function as the primary immunological barrier to
infections. Classically, IgA antibodies prevent the adhesion and penetration of microorganisms to and
through the lining epithelium. Because IgA enters secretions by polymeric immunoglobulin
receptor (pIgR)-mediated endocytosis and transcytosis across epithelial cells, we have proposed that
mucosal IgA has additional host defense functions. One such function is to neutralize intracellular
microbial pathogens, e.g. viruses, that infect mucosal epithelial cells. Intracellular neutralization
of viruses under natural conditions would provide a role for IgA antibody in recovery from infection.
Another proposed function of mucosal IgA is the excretion of antigens from the underlying mucosal
lamina propria. This possibility derives from the fact that receptor mediated endocytosis and transcytosis
of IgA depend on its Fc region, whereas complexing with antigen depends on its Fab regions. Therefore,
the transport of IgA across epithelia is independent of whether the IgA combining sites for antigen are
free, or combined with antigen as an immune complex. Such local excretion of antigens by IgA provides
an internal barrier that helps prevent immune complexes from reaching the systemic circulation. In
these various ways IgA antibodies can defend against infection. Therefore, vaccines designed to stimulate
IgA antibody production offer great potential to combat infections. We are also developing enzyme therapy
for IgA nephropathy, the most common form of glomerulonephritis.
Publications
Lamm ME (1997). Interaction of antigens and antibodies at mucosal surfaces. Annu Rev Microbiol 51, 311-
340.
Huang YT, Miller CJ, Wong V, Nedrud JG, Lamm ME (1999). Replication and budding of simian immunodeficiency virus in polarized epithelial cells. Virology 257, 24-34.
Robinson JK, Blanchard TG, Levine AD, Emancipator SN, Lamm ME (2001). A mucosal IgA-mediated excretory immune system functions in vivo. J Immunol 166:3688-3692.
Emancipator SN, Mestecky J, and Lamm ME. “IgA nephropathy and related diseases” in Mucosal Immunology, 3rd Ed., ed. J. Mestecky, J. Bienenstock, M.E. Lamm, L. Mayer, J.R. McGhee and W. Strober, Elsevier, San Diego, 2005, p. 1580-1600.
Huang YT, Wright A, Gao X, Kulick L, Yan H, and Lamm ME (2005). Intraepithelial cell neutralization of HIV- 1 replication by IgA. J Immunol 174:4828-4835.