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Updated: Jun 23, 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

Anti-TNF-induced lupus.

Emma L Williams1, Stephan Gadola, Christopher J Edwards

  • 1Department of Rheumatology, Southampton General Hospital, Southampton, UK.

Rheumatology (Oxford, England)
|May 7, 2009
PubMed
Summary
This summary is machine-generated.

Anti-TNF-alpha therapies can rarely induce lupus (ATIL), distinct from classical drug-induced lupus. ATIL often involves skin, kidney, or brain and requires careful differentiation from other autoimmune conditions.

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Area of Science:

  • Rheumatology
  • Immunology
  • Pharmacology

Background:

  • Protein-based anti-TNF-alpha therapies are widely used for inflammatory conditions.
  • These therapies commonly induce autoantibodies, but anti-TNF-induced lupus (ATIL) is a rare complication.
  • ATIL exhibits distinct clinical and serological features compared to classical drug-induced lupus (DIL).

Purpose of the Study:

  • To differentiate anti-TNF-induced lupus (ATIL) from other autoimmune conditions.
  • To describe the clinical characteristics and pathogenic mechanisms of ATIL.
  • To guide clinical management of ATIL.

Main Methods:

  • Review of clinical data and literature on ATIL.
  • Comparison of ATIL features with classical drug-induced lupus (DIL).
  • Analysis of potential pathogenic mechanisms and treatment strategies.

Main Results:

  • ATIL can occur with various TNF inhibitors, with differing frequencies and presentations.
  • Cutaneous, renal, and cerebral involvement, along with anti-dsDNA antibodies, are more frequent in ATIL than DIL.
  • ATIL pathogenesis appears distinct from DIL, necessitating careful clinical differentiation from unmasked autoimmune diseases.

Conclusions:

  • ATIL is a rare but distinct entity associated with anti-TNF-alpha therapy.
  • Clinical differentiation from systemic lupus erythematosus (SLE) or connective tissue diseases (CTD) is crucial.
  • Management involves differentiating ATIL, potentially reducing autoantibody formation with immunosuppression, and withdrawing anti-TNF therapy, with steroids for severe cases.