Autoimmunity Branch

Richard Siegel, M.D., Ph.D.
Chief, Autoimmunity Branch
Phone: (301) 496-5767
Fax: (301) 480-3880
E-mail: siegelr@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 Section — Chief, Richard Siegel, M.D., Ph.D.

Selected Publications

Meylan F, Richard AC, Siegel RM. TL1A and DR3, a TNF family ligand-receptor pair that promotes lymphocyte costimulation, mucosal hyperplasia, and autoimmune inflammation. Immunol Rev. 2011 Nov;244(1):188-96.

Ramaswamy M, Deng M, Siegel RM. Harnessing programmed cell death as a therapeutic strategy in rheumatic diseases. Nat Rev Rheumatol. 2011 Mar;7(3):152-60.

Bulua AC, Simon A, Maddipati R, Pelletier M, Park H, Kim KY, Sack MN, Kastner DL, Siegel RM. Mitochondrial reactive oxygen species promote production of proinflammatory cytokines and are elevated in TNFR1-associated periodic syndrome (TRAPS). J Exp Med. 2011 Mar 14;208(3):519-33.

Ramaswamy M, Cruz AC, Cleland SY, Deng M, Price S, Rao VK, Siegel RM. Specific elimination of effector memory CD4(+) T cells due to enhanced Fas signaling complex formation and association with lipid raft microdomains. Cell Death Differ 2011 Apr;18(4):712-20.

Zhang, H.H., K. Song, R.L. Rabin, B.J. Hill, S.P. Perfetto, M. Roederer, D.C. Douek, R.M. Siegel, and J.M. Farber. 2010. CCR2 identifies a stable population of human effector memory CD4(+) T cells equipped for rapid recall response. J Immunol 185:6646-666

Dufour, F., A.M. Sasseville, S. Chabaud, B. Massie, R.M. Siegel, and Y. Langelier. (2010)The ribonucleotide reductase R1 subunits of herpes simplex virus types 1 and 2 protect cells against TNFα- and FasL-induced apoptosis by interacting with caspase-8. Apoptosis online, 10.1007/s10495-010-0560-2

Wang, L., J.K. Yang, V. Kabaleeswaran, A.J. Rice, A.C. Cruz, A.Y. Park, Q. Yin, E. Damko, S.B. Jang, S. Raunser, C.V. Robinson, R.M. Siegel, T. Walz, and H. Wu. (2010) The Fas-FADD death domain complex structure reveals the basis of DISC assembly and disease mutations. Nat Struct Mol Biol 17:1324-1329.

Meylan F, Song YJ, Fuss I, Villarreal S, Kahle E, Malm IJ, Acharya K, Ramos HL, Lo L, Mentink-Kane MM, Wynn TA, Migone TS, Strober W, Siegel RM. The TNF-family cytokine TL1A drives IL-13-dependent small intestinal inflammation. Mucosal Immunology 2011 Mar;4(2):172-85.

Oliveira, J.B., J.J. Bleesing, U. Dianzani, T.A. Fleisher, E.S. Jaffe, M.J. Lenardo, F. Rieux-Laucat, R.M. Siegel, H.C. Su, D.T. Teachey, and V.K. Rao. 2010. Revised diagnostic criteria and classification for the autoimmune lymphoproliferative syndrome (ALPS): report from the 2009 NIH International Workshop. Blood 116:e35-40.

Simon A, Park H, Maddipati R, Lobito AA, Bulua AC, Jackson AJ, Chae JJ, Ettinger R, de Koning HD, Cruz AC, Kastner DL, Komarow H, Siegel RM. Concerted action of wild-type and mutant TNF receptors enhances inflammation in TNF receptor 1-associated periodic fever syndrome. Proc Natl Acad Sci U S A. 2010 May 10. [Epub ahead of print] PubMed PMID: 20457915.

See extended list of publications

Updated October 12, 2010