Ann M Rothstein

Ann M Rothstein is a Professor at UMass Chan Medical School with multiple appointments across the T.H. Chan School of Medicine and Morningside Graduate School of Biomedical Sciences. She holds primary positions in the Department of Medicine (Division of Rheumatology) and Department of Microbiology, while also contributing to the Immunology and Microbiology Program, MD/PhD Program, Postbaccalaureate Research Education Program, and Translational Science department.

Dr. Rothstein's research focuses on fundamental mechanisms of immune regulation in autoimmune diseases. Her laboratory investigates factors regulating T and B lymphocyte activation, function, longevity, and apoptosis, with particular emphasis on animal models of systemic autoimmune disease. She has made significant contributions to understanding how autoantigens that can engage both the B cell receptor and Toll-like receptors (TLR9 or TLR7) activate autoreactive B cells. Her work also examines the dual roles of Fas-ligand in both pro-apoptotic and pro-inflammatory contexts, and she develops animal models of pseudo-GVHD to study tissue-specific immune responses.

Analysis of Dr. Rothstein's publication record reveals consistent research output spanning over 15 years with highly cited papers in immunology. Her most influential work focuses on TLR signaling in autoimmune disease pathogenesis, particularly the mechanisms by which nucleic acid-sensing pathways contribute to systemic lupus erythematosus. Her research bridges basic molecular mechanisms with translational applications for autoimmune disease treatment.

Scientific Awards:

• 2011 Distinguished Lecture, American Association of Immunologists
• 2012 Distinguished Innovator, Lupus Research Institute

Dr. Rothstein maintains an active research program with numerous rotation projects and postdoctoral opportunities focused on the molecular mechanisms of autoreactive B cell activation and innate sensors of cell damage. Her laboratory has established important connections between TLR signaling pathways and autoimmune disease pathogenesis, with potential therapeutic implications for conditions like lupus. She appears to have extensive collaborations across immunology research, as evidenced by her network of co-authors and cited works.

Her laboratory maintains research on three primary fronts: (1) B cell activation by autoantigens engaging both BCR and TLR pathways, (2) regulatory functions of Fas-ligand in inflammation and apoptosis, and (3) animal models of pseudo-GVHD to study tissue-specific immune responses and fibrosis mechanisms.