Tumor necrosis factor alpha (TNF-α), anti-TNF-α and demyelination revisited: An ongoing story

被引：104

作者：

Caminero, Ana ^{[1
,2
]}

Comabella, Manuel ^{[1
]}

Montalban, Xavier ^{[1
]}

机构：

[1] Hosp Univ Vall dHebron, Unitat Neuroimmunol Clin, CEM Cat, Ctr Esclerosi Multiple Catalunya, Barcelona 08035, Spain

[2] Complejo Hosp Avila, Secc Neurol, Avila, Spain

来源：

JOURNAL OF NEUROIMMUNOLOGY | 2011年 / 234卷 / 1-2期

关键词：

Multiple sclerosis; Proinflammatory cytokines; TNF-alpha; Anti-TNF-alpha; EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS; MULTIPLE-SCLEROSIS; FACTOR RECEPTOR; FACTOR THERAPY; HUMAN-DISEASES; MECHANISMS; BLOCKADE; ONSET; INFLAMMATION; PATHOGENESIS;

D O I：

10.1016/j.jneuroim.2011.03.004

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

Tumor necrosis factor alpha (TNF-alpha) is a cytokine with pleiotropic actions that can be present both as a transmembrane protein and soluble cytokine (sTNF). Both ligands interact with two different receptors, TNFR1 and TNFR2, which mediate their biological effects. TNF-alpha is involved in the pathogenesis of multiple sclerosis (MS), however, administration of anti-TNF-alpha agents to MS patients has been associated with increased disease activity. Insomuch as TNFR1 mediates demyelination and TNFR2 remyelination, it could be hypothesized that anti-TNF-alpha agents Which selectively inhibit sTNF or signals from TNFR1 could be effective in treating MS. (C) 2011 Elsevier B.V. All rights reserved.

引用

页码：1 / 6

页数：6

共 57 条

[1] Transmembrane TNF protects mutant mice against intracellular bacterial infections, chronic inflammation and autoimmunity [J].