Regulation of interleukin 2-driven T-lymphocyte proliferation by prolactin

Charles V. Clevenger, Diane H. Russell, Pierette M. Appasamy, Michael B. Prystowsky

Research output: Contribution to journalArticle

208 Citations (Scopus)

Abstract

The requirement for prolactin in interleukin 2-driven T-cell proliferation was evaluated. Addition of an anti-prolactin antiserum resulted in the specific inhibition of T-cell proliferation in a time- and dose-dependent manner. Synthesis of prolactin and its mRNA, however, did not occur during interleukin 2 stimulation. Instead, previously internalized prolactin, presumably from fetal bovine serum, appears to serve as the source of prolactin under serum-free conditions. A 7-fold increase in a prolactin receptor occurred as a function of cell cycle progression; accumulation of a 1.6-kilobase prolactin receptor mRNA increased ≈2-fold. Interleukin 2 stimulation induced the translocation of prolactin into the nucleus and prolactin receptor to the nuclear periphery. These data indicate that extracellular prolactin is requisite for T-cell proliferation and suggest that the effects of prolactin are exerted in the nucleus.

Original languageEnglish (US)
Pages (from-to)6460-6464
Number of pages5
JournalProceedings of the National Academy of Sciences of the United States of America
Volume87
Issue number16
StatePublished - Aug 1990
Externally publishedYes

Fingerprint

Prolactin
Interleukin-2
T-Lymphocytes
Prolactin Receptors
Cell Proliferation
Messenger RNA
Serum
Immune Sera
Cell Cycle

Keywords

  • Cell cycle
  • Flow cytometry
  • Nucleus
  • Prolactin receptor

ASJC Scopus subject areas

  • Genetics
  • General

Cite this

Regulation of interleukin 2-driven T-lymphocyte proliferation by prolactin. / Clevenger, Charles V.; Russell, Diane H.; Appasamy, Pierette M.; Prystowsky, Michael B.

In: Proceedings of the National Academy of Sciences of the United States of America, Vol. 87, No. 16, 08.1990, p. 6460-6464.

Research output: Contribution to journalArticle

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