Dr. Marcus Clark is a nationally known expert in arthritis and autoimmune disease, including rheumatoid and psoriatic arthritis, lupus, scleroderma and osteoarthritis.
Funded by the National Institutes of Health, Dr. Clark’s research examines the key cellular components of the immune process with the goal of understanding the mechanisms and changing the course of autoimmune disease. He is also exploring the role that immune cells play in contributing to the kidney damage sometimes seen in lupus patients.
Dr. Clark is the author of more than 70 peer-reviewed articles in prestigious scientific journals including Science, Nature Immunology, Proceedings of the National Academy of Sciences and the Public Library of Science’s (PLoS) Biology and Immunity.
Dr. Clark attended medical school at the University of California, completed his internship and residency at the University of Michigan, Ann Arbor, and his fellowship at the University of California, San Francisco
Dr. Clark is a member of the American Association of Immunologists, American College of Rheumatology, American Society for Clinical Investigation, and the Henry Kunkel Society.
B Cell Development and Activation: Research Summary
Our laboratory has a long-standing interest in B cell antigen receptor (BCR) signaling and BCR dependent processes regulate specific cell fate decisions. In the bone marrow, we have been working to understand how signals initiated through the BCR, in conjunction with those delivered through the IL-7 receptor, coordinate cell cycle progression with immunoglobulin light chain recombination. In the periphery, we have focused on the molecular mechanisms of receptor endocytosis and endocytic trafficking and how these mechanisms influence BCR trafficking and cell fate. As is the case with our studies of lymphopoiesis, we have derived novel in vivo models, and have performed directed in vitro studies, to obtain definitive insights into these processes. In our newest project area, we are applying our knowledge of B cell biology to understanding how in situ adaptive immune responses drive tubulointerstitial inflammation in human lupus nephritis