Judith Ashouri, MD:

Rheumatoid arthritis (RA) afflicts millions globally, causing significant joint deformity, pain, and functional disability. RA is without cure and its cause is unknown, but CD4 T cells—immune cells widely accepted to play a key role in RA pathogenesis—from patients with RA become activated by proteins through their T cell receptor (called “antigen-specific T cells”) and cause arthritis. Dr. Ashouri’s research uses a unique tool to identify and characterize these antigen-specific T cells in both a mouse model of RA and human RA. Elucidating the contribution of these pathogenic CD4 T cells to arthritis development in RA holds promise for the discovery of improved therapeutic targets.

David Daikh, MD, PhD:

Dr. David Daikh is the Rheumatology Division Chief at the SFVA Medical Center, and director of the rheumatology fellowship program at UCSF. Dr. Daikh’s research focuses on immune mechanisms of rheumatic disease, and he directs a core laboratory that serves a number of investigators at UCSF.

Andrew Gross, MD:

Dr. Andrew Gross directs the Rheumatology Clinic at UCSF Medical Center and in that role he cares for patients with a wide range of rheumatic diseases. Dr. Gross is also involved in facilitating research studies that serve as a bridge between basic science discoveries and results that can be applied to patients who suffer from autoimmune rheumatic disease.

Mehrdad Matloubian, MD:

The goal of Dr. Mehrdad Matloubian’s research is to understand how disease-causing white blood cells find their way to sites of chronic inflammation, such as the joints in rheumatoid arthritis. His hope is that a detailed understanding of the molecular factors that guide white blood cell movement the body will provide an opportunity for pharmaceutical intervention and treatment of many autoimmune diseases.

Mary Nakamura, MD

Dr. Mary Nakamura’s research focuses on a relatively new field called osteoimmunology, which refers to the study of interactions between the skeletal and immune systems. Loss of bone or osteoporosis is a significant problem for patients due to aging but the process is also accelerated by inflammatory and autoimmune diseases yet can also be worsened during therapy for these diseases. Dr. Nakamura’s research in the laboratory focuses on understanding mechanisms that regulate bone loss particularly due to autoimmune disease. In translational studies she is interested in determining factors that predispose rheumatoid arthritis patients to local and systemic bone loss and how bony erosion can be better assessed in patients.

Matija Peterlin, MD:

Dr. Matija Peterlin’s research focuses on how genes are regulated, which concerns primarily those involved in inflammation, autoimmunity, cancer and AIDS. These studies have led to deep insights into basic science and are being translated to human therapy in all these areas.

William Seaman, MD:

Dr. William E. Seaman's research interests include the regulation of immunity and autoimmunity, primarily using mice as a model for human disease. After working in the lab for 35 years, he recently accepted the position of Associate Chair of Medicine for Research at UCSF. A major goal in this position is to facilitate and expand the study of patients within the Department of Medicine, an area where Rheumatology has been a leader, thanks to support by the Rosalind Russell Arthritis Center.

Arthur Weiss, MD, PhD:

Lymphocytes are white blood cells that play central roles in most autoimmune diseases such as rheumatoid arthritis and lupus. Dr. Weiss’ laboratory studies investigate how the intracellular molecular machinery in lymphocytes regulates normal and abnormal responses with an aim towards understanding what goes right during normal immune responses to infections and what goes wrong in autoimmune diseases. Understanding these molecular mechanisms provides valuable information towards developing drugs that target such intracellular machinery.

Julie Zikherman, MD:

Dr. Julie Zikherman is interested in understanding why and how patients with autoimmune diseases such as lupus develop autoantibodies. Using genetic mouse models, she has taken advantage of a new genetic tool that “reports” when and where during and after their development critical signals are encountered by B cells, the source of antibodies.