Jane Parnes
Academic Appointments
- Emeritus Faculty, Acad Council, Medicine - Immunology & Rheumatology
- Member, Stanford Cancer Institute
Key Documents
Contact Information
- Academic Offices
Personal Information Email Tel (650) 723-7038Alternate Contact Sharon Dickow Administrative Assistant Email Tel Work 723-7038
Professional Overview
Honors and Awards
- Wellcome Visiting Professor, Medical College of Virginia (11/92)
- 1991 Young Investigator Award, Western Society for Clinical Investigation (02/91)
- Speaker, Leukemia Society of America Speaker, UCLA (06/89)
- Established Investigator Award, American Heart Association (07/87-06/92)
- Scholar Award (funding declined because of AHA Award), Leukemia Society of America (07/87)
- Faculty Research Award (funding declined because of AHA Award), American Cancer Society (07/87)
Professional Education
| M.D.: | Harvard Medical School, Medicine (1976) |
| A.B.: | Radcliffe College, Cambridge, MA, Biochemical Sciences (1972) |
Graduate & Fellowship Program Affiliations
Scientific Focus
Current Research Interests
CD72 is a B lymphocyte surface protein expressed from early stages of B cell development through to the mature B cell stage, but its expression is turned off as B cells differentiate into plasma cells. To elucidate the function of CD72 we have used gene targeting to generate homozygous mutant mice that totally lack CD72 expression. The B cells in these mice are hyper-responsive to stimulation through the B cell receptor. These data indicate that CD72 plays a negative regulatory role on B cell responsiveness. In accord with our findings, an ITIM motif in the cytoplasmic tail of CD72 has been shown to bind to the tyrosine phosphatase SHP-1, a feature characteristic of other surface proteins that negatively regulate lymphocyte responses. We postulate that CD72 is involved in setting the threshold for B cell responsiveness and that it therefore plays an important role in B cell repertoire selection. Our current studies are examining how CD72 regulates the balance between B cell tolerance and autoimmunity in several model systems. We have evidence that the CD72-deficient mice are more susceptible to the induced autoimmune disease experimental allergic encephalomyelitis, a mouse model of multiple sclerosis. We are studying the mechanisms responsible for the increased severity of disease in CD72-deficient mice. CD72-deficient mice also develop spontaneous autoimmune disease as they age, characterized by production of antinuclear antibodies including anti-single-stranded- and anti-double-stranded-DNA antibodies and eventual development of glomerulonephritis. Current studies are aimed at further characterizing the autoantibodies produced, determining the regulatory changes responsible for their production, as well as their pathogenicity. We are additionally studying the mechanisms by which CD72-deficiency leads to a partial abrogation of B cell anergic tolerance in mice in which all B cells express a transgenic B cell receptor specific for hen-egg lysozyme (HEL) and in which the antigen HEL is expressed in the serum. Finally, the lab is examining the biochemistry of signaling through CD72 to determine the molecular mechanisms by which CD72 regulates B cell responsiveness.
Publications
- CD72 down-modulates BCR-induced signal transduction and diminishes survival in primary mature B lymphocytes. J Immunol. 2006; (9): 5321-8
- Medicine on a need-to-know basis. Nat Immunol. 2006; (6): 543-7
- Mouse splenic B lymphocyte activation using different activation stimuli induces in vitro splicing of tumor necrosis factor-alpha nuclear pre-mRNA. Mol Immunol. 2006; (6): 613-22
- Dual regulation of BCR-mediated growth inhibition signaling by CD72. Eur J Immunol. 2005; (5): 1634-42
- Woodchuck interleukin-6 gene: structure, characterization, and biologic activity. Gene. 2004; (1): 157-64
- OX52 is the rat homologue of CD6: evidence for an effector function in the regulation of CD5 phosphorylation. J Leukoc Biol. 2003; (1): 183-90
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