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Updated: Aug 8, 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

Tumor necrosis factor receptors--structure and function

J Rothe1, G Gehr, H Loetscher

  • 1F. Hoffmann-La Roche, Ltd., Basel, Switzerland.

Immunologic Research
|January 1, 1992
PubMed

Insights

Tumor necrosis factor (TNF) receptors, crucial for cytokine action, have been cloned. Their sequences reveal they belong to the nerve growth factor receptor gene family, aiding understanding of TNF signaling.

Area of Science:

  • Immunology
  • Molecular Biology
  • Cell Biology

Background:

  • Tumor necrosis factors (TNFs) are key cytokines with diverse biological roles.
  • Understanding TNF receptor function is critical for elucidating TNF-mediated cellular responses.

Purpose of the Study:

  • To summarize current knowledge on TNF receptor biochemistry and structure.
  • To report on the molecular cloning of TNF receptor cDNAs.
  • To discuss TNF inhibitory proteins and receptor-mediated signal transduction.

Main Methods:

  • Biochemical characterization of TNF receptors.
  • Molecular cloning of complementary DNAs (cDNAs) for TNF receptors.
  • Sequence analysis of receptor genes.

Main Results:

  • Two distinct types of cell-surface TNF receptors have been identified and cloned.
  • Nucleotide sequence analysis places both TNF receptors within the nerve growth factor receptor gene family.
  • Insights into the structure and function of TNF receptors were gained.

Conclusions:

  • The molecular cloning of TNF receptors provides a foundation for further research into their mechanisms of action.
  • TNF receptors share homology with the nerve growth factor receptor gene family.
  • Further investigation into TNF inhibitory proteins and signal transduction pathways is warranted.

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