The role of the T cell in autoimmune inflammation

Alla Skapenko¹, Jan Leipe², Peter E Lipsky³ and Hendrik Schulze-Koops⁴

¹Research Fellow in Rheumatology, Nikolaus Fiebiger Center for Molecular Medicine, Clinical Research Group III, Department of Internal Medicine III and Institute for Clinical Immunology, University of Erlangen-Nuremberg, Erlangen, Germany

²Medical Student, Nikolaus Fiebiger Center for Molecular Medicine, Clinical Research Group III, Department of Internal Medicine III and Institute for Clinical Immunology, University of Erlangen-Nuremberg, Erlangen, Germany

³Professor, Chief, Autoimmunity Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases, Bethesda, Maryland, USA

⁴Head, Clinical Research Group III, Nikolaus Fiebiger Center for Molecular Medicine, Department of Internal Medicine III and Institute for Clinical Immunology, University of Erlangen-Nuremberg, Erlangen, Germany, and National Institute of Arthritis and Musculoskeletal and Skin Diseases, Bethesda, Maryland, USA

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Arthritis Research & Therapy 2005, 7(Suppl 2):S4-S14doi:10.1186/ar1703


Published:	16 March 2005

Abstract

T cells, in particular CD4⁺T cells, have been implicated in mediating many aspects of autoimmune inflammation. However, current evidence suggests that the role played by CD4⁺T cells in the development of rheumatoid inflammation exceeds that of activated proinflammatory T-helper (Th)1 effector cells that drive the chronic autoimmune response. Subsets of CD4⁺T cells with regulatory capacity, such as CD25⁺regulatory T (Treg) cells and Th2 cells, have been identified, and recent observations suggest that in rheumatoid arthritis the function of these regulatory T cells is severely impaired. Thus, in rheumatoid arthritis, defective regulatory mechanisms might allow the breakdown of peripheral tolerance, after which the detrimental Th1-driven immune response evolves and proceeds to chronic inflammation. Here, we review the functional abnormalities and the contribution of different T cell subsets to rheumatoid inflammation.