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Updated: Sep 26, 2026

Determination of the Relative Potency of an Anti-TNF Monoclonal Antibody (mAb) by Neutralizing TNF Using an In Vitro Bioanalytical Method
16:07

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

Genetic markers for the efficacy of tumour necrosis factor blocking therapy in rheumatoid arthritis

L Padyukov1, J Lampa, M Heimbürger

  • 1Unit of Rheumatology, Karolinska Hospital, Karolinska Institutet, Stockholm, Sweden. leonid.padyukov@cmm.ki.se

Annals of the Rheumatic Diseases
|May 22, 2003
PubMed
Abstract

Insights

Certain genetic variations in cytokine genes correlate with patient response to etanercept treatment for rheumatoid arthritis (RA). These findings may help predict treatment success in RA patients receiving tumor necrosis factor (TNF) blockers.

Area of Science:

  • Immunogenetics
  • Rheumatology
  • Pharmacogenomics

Background:

  • Rheumatoid arthritis (RA) exhibits significant inter-patient variability in treatment response.
  • Tumor necrosis factor (TNF) inhibitors are used for RA, but 20-40% of patients do not respond.
  • Predictive markers for TNF inhibitor response in RA are currently lacking.

Purpose of the Study:

  • To investigate the association between polymorphisms in cytokine genes and patient responsiveness to etanercept, a TNF blocking agent.
  • To identify potential genetic markers for predicting etanercept treatment outcomes in rheumatoid arthritis.

Main Methods:

  • 123 active RA patients were treated with etanercept.
  • Response was assessed at three months using American College of Rheumatology (ACR)20 and Disease Activity Score (DAS)28 criteria.
  • Genotyping was performed for TNF, IL10, TGFbeta1, and IL1RN gene polymorphisms.

Main Results:

  • 20% of patients were classified as non-responders.
  • No single genetic allele was significantly associated with treatment responsiveness.
  • A combination of TNF (-308 TNF1/TNF1) and IL10 (-1087 G/G) alleles was linked to good response (p<0.05).
  • Combined IL1RN (A2 allele) and TGFbeta1 (codon 25 C allele) polymorphisms were associated with non-responsiveness (p<0.05).

Conclusions:

  • Genetic polymorphisms influencing pro- and anti-inflammatory cytokine balance are associated with clinical response to etanercept in RA.
  • These findings suggest potential genetic markers for predicting etanercept efficacy in rheumatoid arthritis patients.

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