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Review
.2011 Jul 26;13(4):232.
doi: 10.1186/ar3376.

Lymphotoxin α revisited: general features and implications in rheumatoid arthritis

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Review

Lymphotoxin α revisited: general features and implications in rheumatoid arthritis

Flavia Calmon-Hamaty et al. Arthritis Res Ther..

Abstract

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.

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Figure 1
Figure 1
Proposed model for the action of lymphotoxin alpha (LTα) in rheumatoid arthritis (RA) fibroblast-like synoviocytes (FLSs). RA FLSs express all LTα receptors (TNFR1, TNFR2, and HVEM). TNFR1 contains a cytoplasmic death domain (DD). Although the specific contribution of each receptor for LTα signaling remains to be clarified, RA FLSs are activated upon LTα binding through the phosphorylation of the mitogen-activated protein kinases p38 and ERK1/2 and of the phosphatidylinositol 3-kinase (PI3K) Akt. Transcription factors such as nuclear factor-kappa-B (NF-κB), in turn, are activated. These events lead to cell responses involved in the pathogenesis of RA, such as proliferation, survival, and secretion of proinflammatory cytokines, chemokines, and matrix metalloproteinases (MMPs). Based on [48]. ERK, extracellular signal-regulated kinase; HVEM, herpesvirus entry mediator; IL, interleukin; JNK, c-jun N-terminal kinase; RANTES, regulated upon activation, normal T cell expressed and secreted; TNFR, tumor necrosis factor receptor.
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