Predictors of response to TNF antagonists
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Updated: Apr 18, 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
Eva Salgado, Jose Ramon Maneiro, Juan J Gomez-Reino1
1Complejo Hospitalario Universitario de Santiago de Compostela, c/ Travesía da Choupana s/n, 15701 Santiago de Compostela, Spain. eva.salgado.perez@gmail.com.
Abstract:
Rheumatoid arthritis (RA) is a chronic inflammatory disease that involves synovial tissue and leads to joint destruction. There are currently 5 tumor necrosis factor (TNF) antagonists licensed for the treatment of RA. This review summarizes the predictors of response to TNF antagonists in RA. Demographic variables were found to predict response, although not consistently. The variables associated with poor clinical response were presence of radiographic joint erosions at baseline, poor functional capacity at baseline, presence of human antibodies against TNF chimeric antibodies, and increase in anti-DNA and antinuclear antibodies. In selected populations, polymorphisms of TNF, TNF receptor, and Fc γ receptor were related to clinical response. Expression of TNF and other inflammatory cytokines in synovial tissue was explored. The heterogeneity of study populations limits the generalizability of the results in most studies.
Insights
Predicting rheumatoid arthritis (RA) treatment response to tumor necrosis factor (TNF) antagonists is complex. Factors like joint damage, functional status, and antibody presence influence outcomes, but results vary across patient groups.
Area of Science:
- Immunology
- Rheumatology
- Pharmacology
Background:
- Rheumatoid arthritis (RA) is a chronic inflammatory joint disease.
- Tumor necrosis factor (TNF) antagonists are key treatments for RA.
- Identifying predictors of TNF antagonist response is crucial for personalized medicine.
Purpose of the Study:
- To review and summarize predictors of clinical response to TNF antagonists in RA patients.
- To explore demographic, immunologic, and genetic factors influencing treatment efficacy.
Main Methods:
- Systematic review of studies on TNF antagonist response in RA.
- Analysis of demographic variables, baseline disease characteristics, and immunologic markers.
- Exploration of genetic polymorphisms and synovial cytokine expression.
Main Results:
- Demographic variables showed inconsistent prediction of response.
- Radiographic joint erosions, poor baseline function, anti-TNF antibodies, and increased anti-DNA/antinuclear antibodies predicted poor response.
- TNF, TNF receptor, and Fc γ receptor polymorphisms were associated with response in specific populations.
- TNF and inflammatory cytokine expression in synovial tissue was examined.
Conclusions:
- Predictors of TNF antagonist response in RA are multifactorial and not fully consistent.
- Baseline disease severity, immunogenicity, and genetic factors play a role.
- Heterogeneity in study populations limits generalizability of findings.
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