Email updates

Keep up to date with the latest news and content from Arthritis Research & Therapy and BioMed Central.

This article is part of the supplement: Basic science, rationale, background and future of abatacept

Highly Accessed Review

The role of the T cell in autoimmune inflammation

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

Author Affiliations

1 Research 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

2 Medical 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

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

4 Head, 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

For all author emails, please log on.

Arthritis Research & Therapy 2005, 7(Suppl 2):S4-S14  doi: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.