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Updated: Jun 3, 2026

Determination of the Relative Potency of an Anti-TNF Monoclonal Antibody (mAb) by Neutralizing TNF Using an In Vitro Bioanalytical Method
Published on: September 16, 2017
Tumor necrosis factor alpha (TNF-α), anti-TNF-α and demyelination revisited: an ongoing story
Ana Caminero1, Manuel Comabella, Xavier Montalban
1Sección de Neurología, Complejo Hospitalario de Avila, Spain.
Tumor necrosis factor alpha (TNF-α) 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-α is involved in the pathogenesis of multiple sclerosis (MS), however, administration of anti-TNF-α 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-α agents which selectively inhibit sTNF or signals from TNFR1 could be effective in treating MS.
Tumor necrosis factor alpha (TNF-α) 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-α is involved in the pathogenesis of multiple sclerosis (MS), however, administration of anti-TNF-α 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-α agents which selectively inhibit sTNF or signals from TNFR1 could be effective in treating MS.
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