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Andrew J. Gross, M.D.

-Assistant Clinical Professor of Medicine
-Director, Rheumatology Clinical Programs


University of California, San Francisco
400 Parnassus Avenue, Plaza Level
San Francisco, CA 94143-0326

Phone: 415-476-5810
Email: ajgross@itsa.ucsf.edu

Dr. Gross received his degree in medicine from Tufts University in 1996. He was trained in internal medicine and rheumatology at Tufts-New England Medical Center, and remained there for another year as a faculty member of the division of rheumatology. Dr. Gross came to UCSF in July 2003 to perform a post-doctoral fellowship in the Department of Microbiology and Immunology and concomenently he joined the faculty of the Division of Rheumatology.

Research Interests

Dr. Gross has two areas of research interest that focus on the deregulation of immune function in systemic lupus erythematosus (SLE).

1. Epstein Barr virus infects nearly all human and establishes a lifelong persistent infection. The virus does not go unchecked though. It seems to be tightly regulated, although the exact mechanisms of this regulation remain uncertain. To further investigate this, Dr. Gross is investigating the effect of SLE on EBV infection. He has found that there is significant deregulation of the virus in these patients, because there are high numbers of infected cells in the blood and abnormal expression of certain EBV genes. This indicates that the immune dysfunction in SLE causes a loss of regulation of the virus. Dr. Gross is now further investigating the mechanisms that cause the breakdown in EBV regulation.

2. When the B-lymphocyte antigen receptor contacts an antigen, a sequence of signals are initiated within the cell. Signaling reactions from the B cell receptor combined with those from other membrane receptors determine the responses of the B cell to the circumstance of its stimulation. Work from Anthony DeFranco’s laboratory at UCSF has shown that mice lacking a central signaling molecule from the Src-family of kinases, Lyn, produce autoantibodies. B cells from these mice have been shown to be hyperresponsive to stimuli. This demonstrates that Lyn has a critical role in several events that downregulate BCR signaling. Dr. Gross, in conjunction with Dr. DeFranco is studying whether autoantibody production is the consequence of Lyn deficiency in B cells alone, or does the absence of Lyn from other immune cells contribute to the development of autoimmunity. Dr. Gross is also studying combinations of factors that are necessary to go from autoantibody production to the development of overt autoimmune disease, i.e. SLE.


R
ecent Publications

Gross AJ, Thorley-Lawson DA. Accumulation of Epstein Barr virus latently infected memory B-lymphocytes in the blood of patients with systemic lupus erythematosus. [Abstract]. American College of Rheumatology, Oct 2002 Annual Scientific Meeting, New Orleans LA.

Gross AJ, Rand W, Hochberg D, Thorley-Lawson DA. EBV and SLE: A New Perspective. In preparation.


   

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