Scripps VIVO scripps research logo

  • Index
  • Log in
  • Home
  • People
  • Organizations
  • Research
  • Events
Search form
As of April 1st VIVO Scientific Profiles will no longer updated for faculty, and the link to VIVO will be removed from the library website. Faculty profile pages will continue to be updated via Interfolio. VIVO will continue being used behind the scenes to update graduate student profiles. Please contact helplib@scripps.edu if you have questions.
How to download citations from VIVO | Alternative profile options

Basis for defective responses of rheumatoid-arthritis synovial-fluid lymphocytes to anti-CD3 (T3) antibodies

Academic Article
uri icon
  • Overview
  • Identity
  • Additional Document Info
  • View All
scroll to property group menus

Overview

authors

  • Lotz, Martin
  • Tsoukas, C. D.
  • Robinson, C. A.
  • Dinarello, C. A.
  • Carson, D. A.
  • Vaughan, J. H.

publication date

  • September 1986

journal

  • Journal of Clinical Investigation  Journal

abstract

  • Synovial fluid mononuclear cells (SFMC) from patients with active rheumatoid arthritis characteristically respond poorly to mitogens. In this study, mitogenic antibodies reactive with the CD3(T3) antigen on human T lymphocytes were used to analyze the basis for the deficiency. OKT3-induced proliferation and release of interleukin 1 (IL-1) and interleukin 2 (IL-2) from SFMC were depressed in all patients. Purified IL-1 or recombinant IL-2 restored proliferative responses in SFMC and increased IL-2 receptor density. Exogenous IL-1 also enhanced IL-2 release. Fractionation of SFMC supernatants on phosphocellulose columns revealed the presence of IL-1 and a potent IL-1 inhibitor. The monocyte-derived IL-1 inhibitor blocked IL-1-dependent responses of normal peripheral blood lymphocytes to OKT3, but had no effect on IL-2-dependent events. These results suggest that IL-1 inhibitor(s) in SFMC impair(s) OKT3-induced mitogenesis by interfering with the effects of IL-1 on T lymphocytes. The net result is deficient IL-2 secretion, IL-2 receptor expression, and impaired cellular proliferation. This novel inhibitory circuit provides a rational explanation for the diminished function of synovial fluid T lymphocytes in rheumatoid arthritis patients.

subject areas

  • Adult
  • Aged
  • Antibodies
  • Antibodies, Monoclonal
  • Antigens, Surface
  • Arthritis, Rheumatoid
  • Cells, Cultured
  • Female
  • Humans
  • Indomethacin
  • Interleukin-1
  • Interleukin-2
  • Lymphocyte Activation
  • Male
  • Middle Aged
  • Monocytes
  • Receptors, Immunologic
  • Receptors, Interleukin-2
  • Synovial Fluid
  • T-Lymphocytes
scroll to property group menus

Identity

International Standard Serial Number (ISSN)

  • 0021-9738

Digital Object Identifier (DOI)

  • 10.1172/jci112631

PubMed ID

  • 3091636
scroll to property group menus

Additional Document Info

start page

  • 713

end page

  • 721

volume

  • 78

issue

  • 3

©2022 The Scripps Research Institute | Terms of Use | Powered by VIVO

  • About
  • Contact Us
  • Support