School of Medicine


Showing 81-90 of 139 Results

  • Eric Meffre

    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.

  • Elizabeth Mellins

    Elizabeth Mellins

    Member, Bio-X

    Current Research and Scholarly InterestsMolecular mechanisms and intracellular pathways of MHC class II antigen processing and presentation, with a focus on B cells; mechanisms underlying HLA allele association with disease; disease mechanisms in systemic juvenile idiopathic arthritis, including an HLA-linked complication; monocytes as drivers or suppressors of auto-inflammation in systemic juvenile idiopathic arthritis and pediatric acute neuropsychiatric syndrome.

  • Maneesh Kumar Misra

    Maneesh Kumar Misra

    Clinical Associate Professor, Pathology

    Current Research and Scholarly InterestsMy research goal is to utilize the cutting edge of stat of art histocompatibility testing to better understand the humoral and cellular responses in clinical transplantation, and to translate this knowledge into improved treatment, and transplant outcome.

  • Daria Mochly-Rosen

    Daria Mochly-Rosen

    George D. Smith Professor of Translational Medicine

    Current Research and Scholarly InterestsTwo areas: 1. Using rationally-designed peptide inhibitors to study protein-protein interactions in cell signaling. Focus: protein kinase C in heart and large GTPases regulating mitochondrial dynamics in neurodegdenration. 2. Using small molecules (identified in a high throughput screens and synthetic chemistry) as activators and inhibitors of aldehyde dehydrogenases, a family of detoxifying enzymes, and glucose-6-phoshate dehydrogenase, in normal cells and in models of human diseases.

  • Stephen B. Montgomery

    Stephen B. Montgomery

    Stanford Medicine Professor of Pathology, Professor of Genetics and of Biomedical Data Science and, by courtesy, of Computer Science

    Current Research and Scholarly InterestsWe focus on understanding the effects of genome variation on cellular phenotypes and cellular modeling of disease through genomic approaches such as next generation RNA sequencing in combination with developing and utilizing state-of-the-art bioinformatics and statistical genetics approaches. See our website at http://montgomerylab.stanford.edu/