Michael E. Lamm, M.D. Professor Emeritus, past Chair of Pathology Mailing Address: 2103 Cornell Rd. WRB 5531 Cleveland, OH 44106-7288 phone: (216) 368-1265 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.