Reverse signaling contributes to control of chronic inflammation by anti-TNF therapeutics

Orsolya Sipos, Annamária Török, Tanja Kalic, Ernő Duda, Kata Filkor

Research output: Contribution to journalArticle

2 Citations (Scopus)


Anti-tumor necrosis factor (TNF) monoclonal antibodies and TNF receptor ectodomain fusion protein are in clinical use to neutralize circulating TNF and ameliorate symptoms of many autoimmune diseases and pathological conditions with chronic inflammation. In this paper we present data to prove that reverse signaling, elicited by agonist molecules interacting with the membrane-bound TNF of myeloid cells, significantly contributes to the therapeutic effect of these anti-TNF medicines. Interaction of agonist monoclonals with cell surface TNF significantly attenuates the expression of pro-inflammatory cytokines and induces changes in the production of extracellular and intracellular signaling molecules. This phenomenon is not dependent on the Fc portion of antibodies as Fab constructs are as efficient as full antibody molecules.

Original languageEnglish
Pages (from-to)123-140
Number of pages18
Issue number2
Publication statusPublished - Jun 9 2015


  • Autoimmune
  • Inflammation
  • Macrophage
  • Monoclonal antibodies
  • Reverse signal
  • TNF receptor
  • Tumor necrosis factor (TNF)

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology
  • Drug Discovery

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