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Volume 2011 (2011), Article ID 810649, 10 pages
Review Article

The Current Concept of T H 17 Cells and Their Expanding Role in Systemic Lupus Erythematosus

1Department of Pathology, Immunology, and Laboratory Medicine, University of Florida, Gainesville, FL 32610, USA
2Department of Oral Biology, College of Dentistry, University of Florida, 1600 SW Archer Road, P.O. Box 100424 Gainesville, FL 32610, USA
3Center for Orphan Autoimmune Disorders, College of Dentistry, University of Florida, 1600 SW Archer Roadd, Gainesville, FL 32610, USA
4Eli and Edythe L. Broad Institute, 7 Cambridge Center, Cambridge, MA 02142, USA
5Department of Chemical Engineering, Massachusetts Institute of Technology, 77 Massachusetts Avenue, E25-545, Cambridge, MA 02139, USA

Received 24 September 2010; Revised 14 December 2010; Accepted 23 January 2011

Academic Editor: G. D. Kitas

Copyright © 2011 Daniel Perry et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Systemic lupus erythematosus (SLE) is a chronic autoimmune disease with a multifaceted range of symptoms affecting almost every organ system. The prototypical pathology of SLE involves the production of antinuclear antibodies and the deposition of immune complexes in basement membranes throughout the body where they induce inflammatory responses. The genetic and environmental etiologies of this process are being intensively sought, and recently, T H 17 cells have been implicated in the pathogenesis of SLE. T H 17 cells are CD4+ memory T cells that behave as both helper and effector cell populations functioning through their signature IL-17 cytokines. Their differentiation is distinct to either the T H 1 or T H 2 cell lineage, but strongly influences development of adaptive responses, including autoimmunity. This paper details the biological functions and regulation of T H 17 cells, followed by an update of their expanding role in SLE.