Biography:
Dr. Tilstra is an Assistant Professor in the Division of Rheumatology and Clinical Immunology at the University of Pittsburgh. He completed his B.S. at the University of Maryland and then completed both his M.D. and his Ph.D at the University of Pittsburgh. His research has focused on lupus nephritis and includes B cell biology, examining immune signaling pathways, and examining the interaction of immune cells and target organs using model organisms.
Dr. Tilstra’s research focuses on lupus nephritis, one of the most severe and common manifestations of systemic lupus erythematosus (SLE). It is estimated that around 40% to 60% of individuals with SLE will develop lupus nephritis at some point during their disease course. Despite the evolution of treatment in this field, remission rates remain low with 10-20% of patients still progressing to end-stage renal disease.
While our comprehension of immune function and lupus has undergone considerable growth over time, there remains a significant gap in our knowledge concerning the intricate processes occurring at the level of the target organ, specifically the kidney. Our research endeavors are aimed at delving into the tissue microenvironment; determining how kidney cells adapt to inflammation and how immune cells change as they infiltrate tissues. We aspire to delineate more precise and effective treatment targets by unraveling the intricate interplay between the immune system and the target organ in lupus nephritis.
Research Summary:
Abnormalities in the immune system play a crucial role in causing organ damage in lupus. Consequently, much of the research community has focused on understanding these immune cells and finding ways to slow down or eliminate them in lupus. However, an area that has received less attention is the study of kidney cells themselves. Previous research indicates that kidney cells undergo changes during lupus nephritis flares, and closely interact with immune cells assumed to cause damage. Therefore, this proposal aims to directly examine kidney cells to understand how they change in lupus nephritis. Additionally, we will investigate whether these changes in kidney cells impact the function of invading immune cells.
Our ongoing studies are examining how kidney tissue responds to immune stimuli and whether this response leads to a protective effect. Preliminary data suggest that kidney tissue responds to inflammation, specifically interferon signaling, by altering the molecules expressed on the surface of kidney cells to suppress invading immune cells. It seems as though the kidney is attempting to protect itself from damage. This proposal will explore whether other inflammatory signals also create protective effects in the kidney and investigate specific ways the tissue may block the function of infiltrating immune cells.
The findings from this proposal will enhance our understanding of why current therapies targeting interferon signaling may not be as effective as anticipated. Additionally, we aim to identify other potential targets that can regulate and halt disease in the target organ without the side effects of targeting all immune cells.
Learn More:
https://profiles.dom.pitt.edu/rheum/faculty_info.aspx/Tilstra6515
