William Cruikshank, Ph.D.
Professor of Medicine
B.S. Washington and Jefferson College
Ph.D. Boston University School of Medicine
For many years my research has centered around the identification, biochemical characterization, cloning, and process of synthesis and secretion of Interleukin-16 (IL-16). Recently we have obtained data indicating that IL- 16 may function in vivo primarily as an immunomodulator. Along those lines, my research is currently focused on the potential role of IL-16, as it relates to several different disease states. IL-16 has direct in vitro bioactivities; induction of CD4+ cell migration, induction of CD4+ lymphocyte cell cycle progression, and prevention of cellular apoptosis which are consistent with proinflammatory cytokines. As such IL-16 has been identified in association with the onset of several inflammatory conditions characterized by the infiltrate of CD4+ cells, such as asthma, sarcoidosis and Crohn’s disease. During the next several years these studies will continue, with particular emphasis on animal models to establish the role of IL-16 in asthma, delayed-type hypersensitivity, and Crohn’s disease.
In addition to the induction of CD4+ cell migration, IL-16 also functions to induce cell cycle progression in peripheral CD4+ T cells and cell differentiation of CD4+ T and B cell stem cells in the bone marrow. In vitro studies have demonstrated that IL-16 stimulation primes the cells for IL-2-induced proliferation. In vivo as well as in vitro studies have identified that IL-16 induces expansion of pre-T and -B cells precursor cells. We are now using the huSCID animal model to determine the efficacy of using IL-16 or IL-16/IL-2 for in vivo immune reconstitution in diseases or therapeutic conditions resulting in CD4+ T cell depletion.