Identification of prolactin as a novel immunomodulator on the expression of co-stimulatory molecules and cytokine secretions on T and B human lymphocytes
We investigate the immunomodulator role of prolactin (PRL) on CD4+ and B cell activation from healthy subjects in comparison with hyperprolactinemic patients. Peripheral blood mononuclear cells, CD4+ or B cells, purified, were cultured under different conditions, as follows: with mitogen, without st...
Veröffentlicht in: | Clinical immunology (Orlando, Fla.). - 1999. - 116(2005), 2 vom: 01. Aug., Seite 182-91 |
---|---|
1. Verfasser: | |
Weitere Verfasser: | , , , , |
Format: | Aufsatz |
Sprache: | English |
Veröffentlicht: |
2005
|
Zugriff auf das übergeordnete Werk: | Clinical immunology (Orlando, Fla.) |
Schlagworte: | Journal Article Research Support, Non-U.S. Gov't Antibodies Antigens, CD Antigens, Differentiation, T-Lymphocyte B7-2 Antigen CD69 antigen CD86 protein, human Cytokines Immunologic Factors mehr... |
Zusammenfassung: | We investigate the immunomodulator role of prolactin (PRL) on CD4+ and B cell activation from healthy subjects in comparison with hyperprolactinemic patients. Peripheral blood mononuclear cells, CD4+ or B cells, purified, were cultured under different conditions, as follows: with mitogen, without stimulus, with different concentrations of human PRL, with unspecific mitogen plus PRL, or with antibodies against PRL. The results revealed that PRL is produced by lymphocytes, the expression of CD69 and CD154 molecules, and interleukin secretions depend partially on the autocrine PRL, this is supported by the findings that secretions of IL-2, IFNgamma, and co-stimulatory molecule expression were markedly reduced when autocrine PRL was blocked with anti-PRL antibodies. Furthermore, PRL activity was only observed during the first 2 h after activation. In contrast, B cell culture did not show any alteration by adding or blocking PRL in the expression of CD40 and CD86 in both groups: healthy subject and hyperprolactinemic patients |
---|---|
Beschreibung: | Date Completed 12.09.2005 Date Revised 01.12.2018 published: Print Citation Status MEDLINE |
ISSN: | 1521-6616 |