Julie Zikherman

Assistant Professor
Department of Medicine
Division of Rheumatology
+1 415 476-1689

Our laboratory is interested in understanding how autoreactive B cells, despite chronic antigen engagement of the B cell receptor, are restrained from inappropriate activation and differentiation. We are interested in how this process is disrupted in autoimmune disease, and how tolerance mechanisms can be harnessed to re-establish tolerance. To do so, we are taking advantage of novel reporter mice in which autoreactive B cells are fluorescently marked (Nur77-eGFP BAC transgenic line). Current funded projects include dissecting the distinct roles of the IgM and IgD B cell receptor isotypes in regulating immune responses by autoreactive B cells. More recent work is focused on defining how Nur77 and related orphan nuclear hormone receptors function selectively to restrain activation of chronically antigen-activated B cells.

Primary Thematic Area: 
Immunology
Secondary Thematic Area: 
None
Research Summary: 
Shaping the B cell repertoire in health and disease

Websites

Featured Publications: 

An extracatalytic function of CD45 in B cells is mediated by CD22.

Proceedings of the National Academy of Sciences of the United States of America

Coughlin S, Noviski M, Mueller JL, Chuwonpad A, Raschke WC, Weiss A, Zikherman J

The role of T cell receptor signaling thresholds in guiding T cell fate decisions.

Current opinion in immunology

Zikherman J, Au-Yeung B

Cutting edge: An in vivo reporter reveals active B cell receptor signaling in the germinal center.

Journal of immunology (Baltimore, Md. : 1950)

Mueller J, Matloubian M, Zikherman J

A sharp T-cell antigen receptor signaling threshold for T-cell proliferation.

Proceedings of the National Academy of Sciences of the United States of America

Au-Yeung BB, Zikherman J, Mueller JL, Ashouri JF, Matloubian M, Cheng DA, Chen Y, Shokat KM, Weiss A