Randy R. Brutkiewicz, PhD
Professor of Microbiology & Immunology
Randy R. Brutkiewicz earned his PhD degree from the University of Massachusetts Medical School and received postdoctoral training at the National Institutes of Health. He is a Professor of Microbiology and Immunology at Indiana University School of Medicine, with an NIH-funded laboratory studying innate immunity, immune evasion and signal transduction pathways.
He was the Associate Dean for Research and Graduate Studies at Indiana University School of Medicine from 2013 - 2017 and oversaw the IU School of Medicine Graduate Division, responsible for graduate and postdoctoral programming and oversight in the IU School of Medicine. An important professional development focus he initiated was the pursuit of nonacademic career paths for trainees.
From 2007 – 2013, Randy Brutkiewicz was an Assistant Dean in the IU School of Medicine Office of Faculty Affairs and Professional Development and a member of the AAMC Group on Faculty Affairs; in 2009, the Office of Faculty Affairs and Professional Development received the AAMC Women in Medicine Leadership Award. Dr. Brutkiewicz’s office was the first of its kind and focused exclusively on research faculty development. His office was responsible for the development, coordination, implementation and oversight of programs aimed at enhancing the development and success of tenure-track and non-tenure track research faculty, and research associates in the School of Medicine.
Microbiology & Immunology
R2 302 950 W. Walnut St.
The Brutkiewicz laboratory studies immune evasion by viruses and tumors as well as the regulation of antigen presentation by various signal transduction pathways, in both innate and adaptive immune responses.
Our studies are mainly focused on the host's innate antiviral and antitumor immune responses. In our laboratory, we study the CD1d molecule, a cell surface glycoprotein that is structurally related to major histocompatibility complex (MHC) class I molecules. These molecules present lipid antigens to a subpopulation of T cells called NKT cells. We have recently reported that the glycolipid α-glucuronosylceramide isolated from the bacterium, Sphingomonas paucimobilis, can activate NKT cells in a CD1d-dependent manner. Our more recent studies have focused on how signal transduction pathways can regulate antigen presentation in both innate (i.e., CD1d) and adaptive (e.g., MHC class II) immune responses. We have found that CD1d-mediated antigen presentation is reciprocally-regulated by the mitogen-activated protein kinases (MAPK), p38 and ERK1/2. This MAPK dichotomy is very evident following a virus infection of antigen presenting cells. Further, we have recently reported that the protein kinase C δ pathway is very critical in the control of antigen presentation by both CD1d and MHC class II (but not MHC class I) molecules. Increasing our understanding of signal transduction pathway control of antigen presentation will be of great help in the development of more effective vaccines against viruses and very useful in the treatment of various hematopoietic tumors, in which the reciprocal regulation of antigen presentation by MAPK is also observed. Our work on NKT cell arm of the host's innate antitumor response has revealed differences between different CD1d+ B and T cell tumors. In the former case, NKT cells are essential, whereas in the latter, NKT cells actually impair the host's protective response. Ongoing studies are analyzing additional mechanisms by which some tumors can evade this arm of the host's innate antitumor defenses, including those signal transduction pathways that play an important role in such activity.
American Association of Immunologists
International Society of Neuroimmunology