Research

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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.


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. PubMed Icon

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. PubMed Icon

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.

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. PubMed Icon

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. PubMed Icon

See complete list of publications

 

Updated December 17, 2007