Randy R. Brutkiewicz, Ph.D.

Associate Professor of Microbiology & Immunology
Associate Member of the Walther Oncology Center

 

Grant Support

Honors

Committees

Editorial Boards

Student Training

Memberships

Training

  • B.S., 1981: Michigan State University
  • Ph.D., 1993: University of Massachusetts Medical Center
  • PostDoctoral, 1993-1998: National Institutes of Health

Positions

  • Associate Professor of Microbiology and Immunology, 1998-present: Indiana University School of Medicine, Indianapolis, IN
  • Associate Member, 1998-present: Walther Oncology Center, Indiana University School of Medicine, Indianapolis, IN

Summary of the research focus:
We study the host's innate antiviral and antitumor immune responses mediated through CD1d/NKT cell interactions.

 

Description and summary of research focus of the laboratory:
We study the host's innate antiviral and antitumor immune responses mediated through CD1d/NKT cell interactions. In our laboratory, we study the CD1d molecule, a cell surface glycoprotein that is structurally related to the major histocompatibility complex (MHC) class I molecules. We have previously found that, unlike MHC class I molecules that present peptides to T cells, a major natural ligand of CD1d molecules is the normal cellular glycolipid, glycosylphosphatidylinositol. We have also previously reported that CD1d molecules are recognized by a unique subpopulation of T cells called NKT cells. Recent work in our laboratory has investigated the intracellular trafficking of CD1d molecules and the intracellular processing requirements necessary for glycolipids to become bound to and presented by CD1d molecules for recognition by NKT cells. We have found that the processing of CD1d-presented glycolipid antigens occurs in a compartment(s) of the endocytic pathway (e.g., endosomes; lysosomes). We are also investigating the role of CD1d molecules and NKT cells in virus infections. A selective loss of NKT cells from the liver and other organs occurs following infection with several different viruses. We believe that this is a protective mechanism--it has been shown that NKT cells can mediate the destruction of liver tissue upon their activation, such as that which occurs following T cell receptor engagement. We are also interested in the role of NKT cells in antitumor immunity. Our recent work has found evidence that shedding of glycolipids by some tumors can inhibit CD1d-mediated antigen presentation to NKT cells. Current studies are analyzing additional mechanisms by which some tumors can evade this arm of the host's innate antitumor defenses.

 

Search Pub Med Listings

 

Scope of Pubilshed Journals:

  • Anticancer Research
  • Blood
  • British Journal of Cancer
  • European Journal of Immunology
  • Hybridoma and Hybridomics
  • Immunity
  • Immunology
  • Immunology and Cell Biology
  • Immunology Letters
  • In Vivo
  • International Journal of Cancer
  • International Journal of Immunotherapy
  • Journal of Experimental Medicine
  • Journal of Immunoassay and Immunochemistry
  • Journal of Immunology
  • Journal of Leukocyte Biology
  • Journal of the National Cancer Institute
  • Journal of Virology
  • Natural Immunity and Cell Growth Regulation
  • Proceedings of the National Academy of Sciences, U.S.A.
  • Science
  • Stem Cells and Development
  • Virology