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The development of B cells into antibody-secreting plasma cells is central to the adaptive immune system as they induce protective and specific antibody responses against invading pathogens. Various studies have shown that, during this process, hormones can play important roles in the lymphopoiesis, activation, proliferation, and differentiation of B cells, and depending on the signal given by the receptor of each hormone, they can have a positive or negative effect. In autoimmune diseases, hormonal deregulation has been reported to be related to the survival, activation and/or differentiation of autoreactive clones of B cells, thus promoting the development of autoimmunity. Clinical manifestations of autoimmune diseases have been associated with estrogens, prolactin (PRL), and growth hormone (GH) levels. However, androgens, such as testosterone and progesterone (P4), could have a protective effect. The objective of this review is to highlight the links between different hormones and the immune response mediated by B cells in the etiopathogenesis of systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), and multiple sclerosis (MS). The data collected provide insights into the role of hormones in the cellular, molecular and/or epigenetic mechanisms that modulate the B-cell response in health and disease., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2024 Santana-Sánchez, Vaquero-García, Legorreta-Haquet, Chávez-Sánchez and Chávez-Rueda.)

Prolactin (PRL) plays an important role in modulating the immune response. In B cells, PRL enhances antibody production, including antibodies with self-specificity. In this study, our aims were to determine the level of PRL receptor expression during bone-marrow B-cell development and to assess whether the presence of high PRL serum concentrations influences absolute numbers of developing populations and disease outcome in lupus-prone murine models. We observed that the PRL-receptor is expressed in early bone-marrow B-cell; the expression in lupus-prone mice, which had the highest level of expression in pro-B cells and immature cells, differed from that in wild-type mice. These expression levels did not significantly change in response to hyperprolactinemia; however, populations of pro-B and immature cells from lupus-prone strains showed a decrease in the absolute numbers of cells with high PRL-receptor expression in response to PRL. Because immature self-reactive B cells are constantly being eliminated, we assessed the expression of survival factor BIRC5, which is more highly expressed in both pro-B and immature B-cells in response to PRL and correlates with the onset of disease. These results identify an important role of PRL in the early stages of the B-cell maturation process: PRL may promote the survival of self-reactive clones.

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.