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Related Experiment Video

Updated: Jun 26, 2026

Determination of the Relative Potency of an Anti-TNF Monoclonal Antibody (mAb) by Neutralizing TNF Using an In Vitro Bioanalytical Method

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

Infliximab and the TNF-alpha system.

Ellen C Ebert¹

¹University of Medicine and Dentistry of New Jersey-Robert Wood Johnson Medical School, New Brunswick, NJ 08903, USA. ebertec@umdnj.edu

American Journal of Physiology. Gastrointestinal and Liver Physiology

|January 13, 2009

Summary

This summary is machine-generated.

Infliximab, an anti-tumor necrosis factor-alpha (TNF-alpha) antibody, enhances anti-inflammatory effects by modulating the TNF-alpha system. It increases soluble TNFR2 release and IL-10 production, promoting an anti-inflammatory microenvironment.

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Determination of the Relative Potency of an Anti-TNF Monoclonal Antibody (mAb) by Neutralizing TNF Using an In Vitro Bioanalytical Method

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Area of Science:

Immunology
Pharmacology

Background:

Infliximab is a monoclonal antibody effective in Crohn's disease (CD) and rheumatoid arthritis (RA).
Its primary mechanism is believed to involve apoptosis induction.
The TNF-alpha system plays a critical role in inflammatory diseases.

Purpose of the Study:

To comprehensively investigate infliximab's effects on the TNF-alpha system.
To analyze these effects in various immune cells from healthy individuals and patients with inflammatory conditions.
To elucidate the molecular mechanisms underlying infliximab's therapeutic action.

Main Methods:

Utilizing peripheral blood monocytes, T cells, and lamina propria lymphocytes.
Studying cells in a resting state to avoid confounding stimuli.
Assessing cell viability, soluble TNFR2 release, TNFR2 expression, TNF-alpha transcript levels, IL-10 production, and c-Jun amino-terminal kinase (JNK) phosphorylation.

Main Results:

Infliximab did not affect cell viability.
It increased soluble TNFR2 release and decreased TNFR2 expression on monocytes, enhancing anti-TNF-alpha activity.
Infliximab promoted IL-10 production while suppressing pro-inflammatory cytokines and increased monocyte JNK phosphorylation.

Conclusions:

Infliximab effectively modulates the TNF-alpha system to exert its anti-inflammatory and therapeutic effects.
The drug enhances the neutralization of TNF-alpha and promotes an anti-inflammatory milieu.
These findings provide a deeper understanding of infliximab's mechanism of action in immune-mediated diseases.