Stanford University
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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. -
Alisa Mueller, MD, PhD
Assistant Professor of Medicine (Immunology and Rheumatology)
BioDr. Mueller is an Assistant Professor in the Division of Immunology and Rheumatology. As a physician-scientist, she leads a research laboratory investigating mechanisms that drive stromal pathology in rheumatoid arthritis and other chronic inflammatory conditions. Utilizing innovative techniques in immunology, genomics, and regenerative medicine, she and her team aim to develop novel therapeutic approaches to combat autoimmune diseases.
Dr. Mueller earned her MD and PhD degrees at Stanford University as part of the Medical Scientist Training Program where she investigated mechanisms regulating a mesenchymal progenitor population in skeletal muscle that mediates both healthy tissue regeneration and pathologic fibrosis. During her training, she was awarded predoctoral grants from the NIH National Institute on Aging and the California Institute of Regenerative Medicine. Her studies culminated in a first-author publication in Nature and co-authorship on publications in Cell and Nature Communications. Subsequently, she pursued medicine residency and rheumatology fellowship at Brigham and Women’s Hospital and Harvard Medical School where she explored mechanisms driving synovial fibroblast pathogenicity in rheumatoid arthritis. Her work led to the identification of non-canonical Wnt signaling as a critical mediator of RA synovial fibroblast inflammatory activation as well as the development of functional genomic screens to elucidate a broad set of novel therapeutic targets in inflammatory fibroblasts. Moreover, she has also led high-dimensional immunoprofiling studies to reveal underlying immune aberrations in patients with systemic sclerosis and elucidate biologic mechanisms catalyzing disease in patients with longstanding immune-related disorders of unknown etiology in partnership with the Undiagnosed Diseases Network. During her fellowship and instructorship, she received a Distinguished Fellow Award from the American College of Rheumatology as well as grants including the NIH NIAMS Mentored Clinical Scientist Research Career Development Award (K08), Rheumatology Research Foundation Scientist Development Award with the Malawista Endowment Distinction, Hearst Young Investigator Award, and Innovation Evergreen Fund Award. Her work has resulted in co-first author publications in the Journal of Clinical Investigation, Cell Reports Medicine, and ACR Open Rheumatology as well as as co-authorship on publications in Lancet Rheumatology and the New England Journal of Medicine.
In addition to her scientific endeavors, Dr. Mueller is also dedicated to providing high quality clinical care and education. She serves as an attending physician specializing in rheumatology where she mentors trainees in outpatient and inpatient settings and provides educational lectures. With an interdisciplinary team, she developed an interactive medical case on neurologic manifestations of lupus which was published in the New England Journal of Medicine. She was awarded an Arnold Dunne Award for Compassion and Dedication to Patient Care at Brigham and Women’s Hospital. By pursuing basic and translational research alongside clinical care, Dr. Mueller and her team strive to uncover basic mechanisms regulating stromal biology in autoimmune and inflammatory disease development and to create diagnostic strategies and targeted therapeutics that will benefit patients who do not respond to conventional therapies.
