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

Abstract

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.

Downregulation of CD94/NKG2A Inhibitory Receptor on Decreased γδ T Cells in Patients with Systemic Lupus Erythematosus

“…CD69 is an early activation‐associated marker of T cells [10], while HLA‐DR is associated to late stage activation [11]. CD25 expression is upregulated upon the initial encounter with specific antigen on T lymphocytes [12]. Here, we found significantly increased percentage of CD69 + and HLA‐DR + γδ T cells in patients with SLE.…”

Immune‐Neuroendocrine Interactions and Autoimmune Diseases

“…Both IL-2 and IL-4 reduced PRL mRNA levels in T lymphocytes (Gerlo et al 2005). PRL significantly enhanced the expression of CD69, CD25 and CD154 and cytokines secretion, and modulate B cells development (Morales et al 1999;Takizawa et al 2005). Therefore, PRL has an important role in adaptive immune response.…”

Prolactin down-regulates CD4+CD25hiCD127low/− regulatory T cell function in humans

“…During an immune response, PRL promotes the proliferation and differentiation of T cells (Carreño et al 2005) and influences the expression of CD69 and CD154 in CD4 C T cells (Chávez-Rueda et al 2005. In addition, when CD8 C T cells are co-incubated with PRL and phytohaemagglutinin, CD69 expression increases (Takizawa et al 2005). In CD4 C T cell cultures activated with phorbol myristate acetate and incubated with an anti-PRL antibody, reduced secretion of IL2 and IFNg is observed, indicating a role for PRL in the regulation of cytokine secretion (Chávez-Rueda et al 2005).…”