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Lymphotoxin α revisited: general features and implications in rheumatoid arthritis

Flavia Calmon-Hamaty1, Bernard Combe123, Michael Hahne14 and Jacques Morel123*

Author affiliations

1 Institut de Génétique Moléculaire de Montpellier CNRS-UMR 5535, 1919 Route de Mende, 34293 Montpellier, Cedex 5, France

2 Department of Rheumatology, Hôpital Lapeyronie, 371 Avenue du Doyen Gaston Giraud, 34295 Montpellier, Cedex 5, France

3 University of Montpellier 1, 2 Rue École de medicine CS 59001, 34060 Montpellier, Cedex 2, France

4 University of Montpellier 2, Route de Mende, 34199 Montpellier, Cedex 5, France

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Citation and License

Arthritis Research & Therapy 2011, 13:232  doi:10.1186/ar3376

Published: 26 July 2011


Rheumatoid arthritis (RA) is a chronic inflammatory disease affecting synovial joints. Therapies blocking tumor necrosis factor-alpha (TNFα) are now routinely used in the management of RA. However, a significant number of patients with RA do not respond or develop resistance to anti-TNF therapies, and the participation of other cytokines in RA pathogenesis has been reported as well. Lymphotoxin alpha (LTα) is the closest homolog to TNFα and has been implicated in inflammation and autoimmunity since its original description in 1968. In spite of that, little is known about the role of LTα in RA or the potential of blocking this cytokine as an alternative therapeutic approach. In this review, we aim to summarize the general features of LTα and what is currently known about its participation in RA.