Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 1987 Oct 1;139(7):2355-60.

Reconstitution of a functional interleukin 2 receptor in a nonlymphoid cell

Affiliations
  • PMID: 2821112

Reconstitution of a functional interleukin 2 receptor in a nonlymphoid cell

L A Rubin et al. J Immunol. .

Abstract

The maintenance of T lymphocytes which are important effectors of immune responses requires the T cell growth factor, interleukin 2 (IL-2). The binding of IL-2 to specific cell-surface receptors (IL-2R) has previously been shown to be essential to the growth and proliferation of activated lymphocytes. A human IL-2R cDNA sequence, placed under the control of the SV40 transcriptional promoter and enhancer, has been transfected into murine L cells. Single cell analysis by autoradiography was used to show that fibroblastic L cells, stably expressing human IL-2R, respond to stimulation with IL-2 by DNA synthesis and proliferation. This response is specifically blocked by the addition of an anti-IL-2R monoclonal antibody, anti-Tac, as previously reported. Neither nonspecific antisera nor 7G7/B6, an anti-IL-2R monoclonal antibody which does not interfere with IL-2 binding to its receptor, had any effect on this response. The induction of DNA synthesis by IL-2 is both rapid and dose-dependent. The ability of IL-2 to stimulate these transfected L cells to proliferate demonstrates that a lymphoid environment is not required for the functional interaction between IL-2 and its receptor, and provides a unique model system for the investigation of the molecular basis for the cellular events mediated by IL-2.

PubMed Disclaimer

Similar articles

Cited by

MeSH terms

LinkOut - more resources