Prolactin Induction of Interleukin-2 Receptors on Rat Splenic Lymphocytes*

Mukherjee, Pinku; Mastro, Andrea M.; Hymer, W. C.

doi:10.1210/endo-126-1-88

Cited by 173 publications

(47 citation statements)

References 21 publications

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“…However, receptors for prolactin (24) and growth hormone (24), which also activate Stat5, are present on lymphoid cells (25)(26)(27). Prolactin increases proliferation of lymphocytes (28,29) and enhances IL-4 production (30).…”

Section: Il-2 Is Important In Th2 Primingmentioning

confidence: 99%

Interleukin 2 plays a central role in Th2 differentiation

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Foucras

Guo

et al. 2004

Proc. Natl. Acad. Sci. U.S.A.

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Section: Il-2 Is Important In Th2 Primingmentioning

confidence: 99%

Interleukin 2 plays a central role in Th2 differentiation

Cote-Sierra

Foucras

Guo

et al. 2004

Proc. Natl. Acad. Sci. U.S.A.

353

358

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“…Alternatively, PRL could act indirectly by upregulation of the expression of cytokine receptors, such as IL-2 receptor alpha (IL-2Ra, CD25) as reported for rat splenocytes Revised 24 October 2002; accepted 22 January 2003 (Mukherjee et al, 1990) and for mouse CD4 + and CD8 + T cells (Gala and Shevach, 1993). Prolactin could also upregulate expression of its own receptor on human peripheral blood lymphocytes (Dardenne et al, 1994), including T cells (O'Neal et al, 1991).…”

mentioning

confidence: 99%

Role of prolactin receptor and CD25 in protection of circulating T lymphocytes from apoptosis in patients with breast cancer

et al. 2003

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Prolactin (PRL) has been reported to inhibit apoptosis in various cell types and to serve as a cofactor in the upregulation of CD25 on T cells during activation. We investigated a possible relation between prolactin receptor (PRL-R) or IL-2 receptor alpha (IL-2Ra, CD25) expression on circulating T lymphocytes and their apoptosis in patients with breast cancer. Peripheral blood mononuclear cells obtained from 25 patients, 25 normal controls (NC) and three cord blood samples were evaluated for Annexin V binding and expression of CD95, CD25, and PRL-R on CD3 + T cells by multicolour flow cytometry. Plasma levels of PRL, sCD95L, and sIL-2R were determined in patients and controls and related to T-cell apoptosis. The ability of PRL to protect T cells from apoptosis induced by various agents was also studied. Expression of PRL-R on the surface of T cells was comparable in patients with breast cancer and NC, but PRL plasma levels in patients were significantly lower (Po0.05). In patients, 18711% (mean7s.d.) of CD3 + cells bound Annexin V, compared to 976% in NC (Po0.0004). Percentages of CD3 + Fas + and CD3 + CD25 + cells were higher in the peripheral circulation of patients than NC (Po0.0001 and o0.04, respectively). Levels of sFasL were lowest in plasma of the patients with the highest proportions of CD3 + Fas + T cells. Most T cells undergoing apoptosis were CD3 + CD25 À in patients, and the proportion of CD3 + CD25 À Annexin V + cells was significantly increased in patients compared to NC (Po0.006). Ex vivo PRL protected T cells from starvation-induced or anti-CD3Ab-induced but not from Fas/FasL-dependent apoptosis. These results indicate that expression of CD25 but not of PRL-R on the surface of activated T lymphocytes appears to be involved in modulating Fas/Fas -ligand interactions, which are, in part, responsible for apoptosis of T lymphocytes and excessive turnover of immune cells in the circulation of patients with breast cancer.

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“…Russell et al [7] have identified PRL receptors on human PBMCs and have indicated that they were specific for PRL. It has already been reported that PRL could induce IL-2 receptor (CD25) expression in murine lymphocytes [9,10], but the effect of PRL on the expression of CD25 and other activation markers in human lymphocytes has rarely been evaluated. In this paper, we have shown that PRL could significantly enhance the expression of CD69 and CD25 antigen on human PBMCs.…”

Section: Discussionmentioning

confidence: 99%

“…The proliferative response of mouse spleen cells exposed to Con-A was significantly potentiated by PRL [12]. Ornithine decarboxylase (ODC) in human lymphocytes [7] and the formation of IL-2 cell surface receptors on lymphocytes [9,10,13] were induced by PRL. In our experiment, PRL at 1-2 mg/ml significantly enhanced the expression of CD69 and PRL at 0.2-1 mg/ml significantly enhanced the expression of CD25 induced by PHA stimulation, respectively, but PRL alone did not induce the expression of CD69 and CD25.…”

Section: Discussionmentioning

confidence: 99%

“…In patients with rheumatoid arthritis (RA), synovium infiltrating T cells which play an important role in the pathogenesis, might synthesize PRL in situ [15]. Moreover, PRL is produced by PBMCs as well as the anterior pituitary gland [7][8][9]. On the other hand, several reports have suggested that PRL in high concentrations is immunosuppressive.…”

Section: Discussionmentioning

confidence: 99%

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Enhanced Expression of CD69 and CD25 Antigen on Human Peripheral Blood Mononuclear Cells by Prolactin

et al. 2005

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Abstract. Several clinical reports have suggested that prolactin (PRL) plays an important role in the pathogenesis of autoimmune diseases such as rheumatoid arthritis (RA) or systemic lupus erythematosus (SLE). We have investigated the influence of PRL on immune system, by evaluating the effects of PRL on the expression of CD69 and CD25 on human peripheral blood mononuclear cells (PBMCs). Human PBMCs obtained from healthy female volunteers were incubated with phytohemagglutinin (PHA) in the presence or absence of various concentrations of PRL. The expression of CD69 and CD25 was monitored using immunofluorescence staining and flow cytometry. PRL significantly enhanced the expression of CD69 and CD25 on activated PBMCs compared with that in the absence of PRL (p<0.05, paired t-test). Increasing doses of PRL enhanced the expression of CD69 up to 2 mg/ml and CD25 up to 1 mg/ml. The enhanced expression of CD69 was observed on CD8+ T lymphocytes but not on CD4+ T lymphocytes. Our data suggest that PRL can significantly enhance the expression of CD69 and CD25 molecule on human PBMCs when induced by PHA. However, PRL would have to be at optimal concentration in order to enhance their expression. PROLACTIN (PRL) is a pituitary hormone which is known to induce the synthesis of milk proteins in women during breastfeeding [1]. Of particular interest, however, is the role of PRL in immune regulation. Evidence suggests that the immune system is an important target of pituitary PRL, and that PRL may play a physiological role in the regulation of cell-mediated and humoral immune response [2]. It has been shown that PRL has an important role in regulating T lymphocyte-mediated immune functions [3,4]. Receptors for PRL on human lymphocytes have been identified on T and B lymphocytes [5][6][7].On the other hand, T lymphocytes express de novo several cell surface glycoproteins, which are also called activation inducer molecules, in a characteristic order during activation. CD69, one of the earliest of the cell surface activation markers, is a phosphorylated 28-32-kilodalton disulphide linked homodimer. Once expressed, CD69 is thought to take part in the ongoing activation process. CD25 (the a chain of the IL-2 receptor), a phosphorylated 55-60-kilodalton cell surface glycoprotein, is also an activation marker induced during lymphoid cell activation. The synthesis of CD25, along with the IL-2 itself, is induced by the activation of T lymphocytes on the initial encounter with specific antigen. In this report, we have examined the effects of PRL on the expression of CD69 and CD25 antigen on human peripheral blood mononuclear cells (PBMCs). We have found that exogenously-added PRL could significantly enhance the expression of CD69 and CD25 antigen on human PBMCs.

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Prolactin Induction of Interleukin-2 Receptors on Rat Splenic Lymphocytes*

Cited by 173 publications

References 21 publications

Interleukin 2 plays a central role in Th2 differentiation

Interleukin 2 plays a central role in Th2 differentiation

Role of prolactin receptor and CD25 in protection of circulating T lymphocytes from apoptosis in patients with breast cancer

Enhanced Expression of CD69 and CD25 Antigen on Human Peripheral Blood Mononuclear Cells by Prolactin

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