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Research
Autoimmunity Branch
Paul Plotz, M.D.
Acting Chief, Autoimmunity Branch
Phone: (301) 594-0596
Fax: (301) 402-2209
E-mail: plotzp@mail.nih.gov
Autoimmunity is a central feature of many rheumatic diseases, such as systemic lupus erythematosus, rheumatoid arthritis, and dermatomyositis. The Autoimmunity Branch was established to address the cellular and molecular basis of autoimmunity. A number of work groups have been established within the Autoimmunity Branch to investigate specific aspects of immune cell function as they may pertain to the etiology of autoimmunity.
- Immunoregulation Group — Group Leader, Richard Siegel, M.D., Ph.D.
- Repertoire Analysis Group — Group Leader, Paul Plotz, M.D.
Selected Publications
Meylan F, Davidson TS, Kahle E, Kinder M, Acharya K, Jankovic D, Bundoc V, Hodges M, Shevach EM, Keane-Myers A, Wang EC, Siegel RM. The TNF-family receptor DR3 is essential for diverse T cell-mediated inflammatory diseases. Immunity. 2008 Jul;29(1):79-89. Epub 2008 Jun 19.
Madhu Ramaswamy, Celine Dumont, Anthony C. Cruz, Jagan R. Muppidi, Timothy S. Gomez, Daniel D. Billadeau, Victor L.J. Tybulewicz, and Richard M. Siegel. (2007) Cutting Edge: Rac GTPases sensitize activated T cells to die via Fas. J. Immunol, in press.
Liu, E.H., Siegel, R.M., Harlan, D.M., and O'Shea, J.J. 2007. T cell-directed therapies: lessons learned and future prospects. Nat Immunol 8: 25-30.
Lobito, A.A., F.C. Kimberley, J.R. Muppidi, H. Komarow, A.J. Jackson, K.M. Hull, D.L. Kastner, G.R. Screaton, and R.M. Siegel. 2006. Abnormal disulfide-linked oligomerization results in ER retention and altered signaling by TNFR1 mutants in TNFR1-associated periodic fever syndrome (TRAPS). Blood.108:1320-7.
Muppidi JR, Siegel RM. Ligand-independent redistribution of Fas (CD95) into lipid rafts mediates clonotypic T cell death. Nat Immunol. 2004 Feb;5(2):182-9. Epub 2004 Jan 25.
See complete list of publications
Updated December 17, 2007