Dr. Finkelman's group’s contributions to immunology and medicine have focused on the use of mouse models of normal and abnormal immune function. They have included the initial demonstrations that: 1) IL-4 is required for induction of IgE responses in vivo, IFN-γ promotes the induction of IgG2a responses in vivo, and IL-12 suppresses IgE responses in vivo; 2) IL-4, IL-13, IL-4Rα, and Stat6 are required for host protection against intestinal worms, and protect predominantly through effects on intestinal epithelial cells, including induction of RELMβ; 3) inflammatory stimuli are required to induce dendritic cells to present antigen in a stimulatory, rather than a tolerogenic fashion; 4) complement and macrophages are required for development of murine transfusion-related acute lung injury; 5) rapid desensitization with anti-FcεRIα monoclonal antibody is a safe and effective way to rapidly suppress IgE-mediated disorders; and 6) immunoglobulin isotypes that are relatively ineffective in the induction of antibody effector mechanisms protect against inflammatory disease.
In addition, his group has developed three important in vivo techniques: 1) the use of anti-IgD antibodies to stimulate polyclonal B cell and T cell activation and antibody secretion; 2) the use of cytokine/anti-cytokine monoclonal antibody complexes to induce long-lasting increases in cytokine effects; and 3) the in vivo cytokine capture assay for measurement of in vivo cytokine secretion.
BA: Queens College, Queens, NY, 1967.
MD: Yale University School of Medicine, New Haven, CN, 1971.
Residency: Internal Medicine, Yale-New Haven Hospital, New Haven, CN.
Fellowship: Laboratory of Immunology, NIAID, NIH, Bethesda, MD.
Fellowship: Rheumatology, University of Texas-Southwestern Medical School, Dallas, TX.
Certification: Internal Medicine, 1976; Rheumatology, 1980.
Internal medicine; rheumatology
Cytokine and antibody roles in disease and host protection.