Regulation of interleukin 2-driven T-lymphocyte proliferation by prolactin.
AUTOR(ES)
Clevenger, C V
RESUMO
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 approximately 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.
ACESSO AO ARTIGO
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=54554Documentos Relacionados
- Transfer of murine host protection by using interleukin-2-dependent T-lymphocyte lines.
- Transfer of Murine Host Protection by Using Interleukin-2-Dependent T-Lymphocyte Lines
- Regulation of human T-lymphocyte gene expression by interleukin 2: immediate-response genes include the proto-oncogene c-myb.
- Enhanced alveolar macrophage-mediated antigen-induced T-lymphocyte proliferation in sarcoidosis.
- T-lymphocyte subpopulations in uveitis.