Lloyd Stoolman, M.D.

Professor of Pathology
Director, Flow Cytometry


Dr. Stoolman received his undergraduate degree from Princeton University, Princeton, New Jersey, in 1972 and his M.D. from the University of California San Francisco (UCSF) in 1977. After an internship and residency in Anatomic Pathology and Laboratory Medicine at UCSF from 1977-1982, including a Chief Residency in Laboratory Medicine, he took a fellowship at UCSF in Anatomy/Cell Biology during 1982-1983.

In 1983, Dr. Stoolman joined the University of Michigan Department of Pathology as an Assistant Professor and Attending Physician for the Flow Cytometry Laboratory. In 1987, he became the Co-Director of the Clinical Flow Cytometry Laboratory. He was promoted to the rank of Associate Professor in 1991. Among many other responsibilities, from 1996 to the present, Dr. Stoolman has been the Director of the Laboratory Sequence in General Pathology for Dental and Graduate Students, where he has developed a Web-based interactive courseware for that Laboratory Sequence.

Dr. Stoolman’s major clinical and research interests are in the areas of hematology, flow cytometry, and immunopathology. He is the Principal Investigator for several current NIH projects, as well as numerous other NIH projects since 1984. He has performed editorial roles for many scientific publications and is currently an Associate Editor for the Journal of Immunology.

Research Interests

White blood cells are the cellular elements of both the innate and acquired immune systems. The trafficking of these cells from the bloodstream into tissues is at the core of both normal and pathologic inflammation. Transient, self-limited trafficking into tissues is essential for the clearance of extra- and intracellular pathogens and the suppression of neoplastic diseases. However, prolonged or excessive leukocyte trafficking damages healthy tissues in autoimmune diseases, hypersensitivity disorders and organ transplant rejection. My laboratory investigates the molecular basis, regulation and clinical ramifications of leukocyte trafficking in health and disease. Current active or planned areas of study include: (1) the regulation of adhesion receptor synthesis on cancer-specific effector T-cells developing in lymph nodes draining viable tumors and tumor-vaccination sites; (2) the mechanism governing the trafficking of circulating, tumor-specific effector cells into primary and metastatic cancers, (3) the development of novel cellular immunotherapy approaches for metastatic cancer based on a detailed understanding of effector T-cell trafficking, (4) the regulation of effector T-cell trafficking during normal and pathologic cell-mediated immunologic reactions in vivo and (5) the development and testing of novel inhibitors of the selectin family of adhesion receptors. Investigators will have the opportunity to study a variety of topics in cellular immunology including tumor immunology, cellular immunotherapy, basic mechanisms of leukocyte adhesion and recruitment and the molecular basis of organ selective lymphocyte trafficking.


Wagers, A.J., Waters, C.M., Stoolman, L.M., Kansas, G.S., Interleukin 12 and interleukin 4 control T cell adhesion to endothelial selectins through opposite effects on alpha1, 3-fucosyltransferase VII gene expression. Journal of Experimental Medicine 188(12):2225-31, 1998.

Knibbs, R.N., Craig, R.A., Maly, P., Smith, P.L., Wolber, F.M., Faulkner, N.E., Lowe, J.B., Stoolman, L.M. Alpha(1,3)-fucosyltransferase VII-dependent synthesis of P- and E- selectin ligands on cultured T lymphoblasts. Journal of Immunology 161(11):6305-15, 1998.

Wolber, F.M., Curtis, J.L., Maly, P., Kelly, R.J., Smith, P., Yednock, T.A., Lowe, J.B., Stoolman, L.M. Endothelial selectins and alpha4 integrins regulate independent pathways of T lymphocyte recruitment in the pulmonary immune response. Journal of Immunology 161(8):4396-403, 1998.

Wolber, F.M., Curtis, J.L., Milik, A.M., Fields, T., Seitzman, G.D., Kim, K., Kim, S., Sonstein, J., Stoolman, L.M. Lymphocyte recruitment and the kinetics of adhesion receptor expression during the pulmonary immune response to particulate antigen. American Journal of Pathology 151(6):1715-27, 1997.

Past Student Advisees