School of Medicine
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Eric Meffre
Professor of Medicine (Immunology and Rheumatology)
BioDr. Meffre obtained his PhD in Immunology from the Université d’Aix-Marseille in France before he moved to the USA as a postdoc fellow in the laboratory of Dr. Michel Nussenzweig at The Rockefeller University in New York City. He became an assistant professor at Cornell University in 2003 before being recruited at Yale University as associate professor in 2009. He was tenured at Yale in 2014 before he joined the Department of Medicine/Division of Immunology and Rheumatology at Stanford University as a tenured full professor in 2022.
Dr. Meffre’s work focuses on the etiology of autoimmune syndromes and the roles played by B cells in these diseases. His group characterized the abnormal selection of developing autoreactive B cells in patients with rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), type 1 diabetes (T1D), multiple sclerosis (MS) and Sjögren’s syndrome, resulting in large numbers of autoreactive naïve B cells accumulating in the patient’s blood. Hence, these autoreactive B cells may present self-antigens to T cells and initiate autoimmune diseases. These early B cell tolerance defects are likely primary to these autoimmune diseases and may result from genetic factors such as the 1858T PTPN22 allele that segregates with RA, SLE and T1D and correlate with an impaired removal of developing autoreactive B cells.
His research goals also consist in characterizing the molecules and pathways involved in the establishment of B cell tolerance and the removal of developing autoreactive B cells generated by random V(D)J recombination through the investigation of rare patients with primary immunodeficiency (PID) enrolled through an international network. Alteration of B cell receptor (BCR) or Toll-like receptor (TLR) signaling in PID patients results in a defective central B cell tolerance and a failure to counterselect developing autoreactive B cells in the bone marrow. In contrast, functional and suppressive regulatory T cells play a key role in preventing the accumulation of autoreactive clones in the mature naïve B cell compartment. The recent development of humanized mouse models recapitulating early B cell tolerance checkpoints and their defects in autoimmune settings allow further in-depth investigation of tolerance mechanisms and the development of novel approaches to restore defective central and peripheral B cell tolerance checkpoints and thwart autoimmunity. -
Salvinaz Islam Moutusy
Postdoctoral Scholar, Immunology and Rheumatology
BioI am a medical scientist with expertise in basic biomedical research focusing on Microbiology and Immunology. After getting medical license from Bangladesh, I received MD in Medical Microbiology from BSMMU, Bangladesh and MS in Environmental Health Science from the University of Tokyo School of Medicine, Japan.
