Potentiation of antibody responsiveness after the transplantation of a syngeneic pituitary gland

doi:10.1016/0165-5728(89)90083-0

Journal of Neuroimmunology

Volume 25, Issue 1, November 1989, Pages 29-35

https://doi.org/10.1016/0165-5728(89)90083-0 Get rights and content

Abstract

Transplantation of a pituitary graft under the kidney capsule and the resulting elevation of serum prolactin enhances the primary humoral antibody response to sheep red blood cells. Enhancement of the response is not due to marked changes in the percentage of T-cells and their subsets, B-cells, or the number of nucleated spleen cells. Quantitation of serum prolactin levels correlates well with the proportion of enhancement as mice with two grafts and higher levels of prolactin have increased responsiveness compared to mice with one graft. Systemic administration of mouse prolactin at the time of immunization also enhances the humoral immune response; however, if prolactin treatment is delayed and given 24 h after immunization, no potentiation of the response occurs. Thus, prolactin is enhancing the immune response by affecting an early afferent event in the induction of the immune response.

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Thus, the increase in prolactin levels during pregnancy may attenuate the potentially harmful effects of the increased glucocorticoid levels on levels of apoptosis of lymphocytes. Prolactin regulates the production of cytokines by T cells (Dimitrov et al., 2004), and also augments the estrogen-derived shift of the balance of the immune response during pregnancy so that humoral immunity (T helper type II lymphocytes) predominates over cell-mediated immunity (T helper type I lymphocytes) (Cross et al., 1989; Gaunt and Ramin, 2001; Ijaz et al., 1990; Szekeres-Bartho, 2002). This shift away from cell-mediated immunity assists in the lack of immune response to the paternally-derived fetal antigens permitting implantation and continuance of the pregnancy.
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Prolactin, a peptide hormone, has the potential to stimulate the immune system and has been implicated as a factor that can activate autoimmune diseases. Prolactin is produced in the anterior pituitary as well as extrapituitary sites such as the brain and lymphocytes5 and is a cytokine, with comparable structural motifs and similar receptor structures and signal transduction pathways. Prolactin receptors are distributed throughout the immune system and are included in a novel receptor family that includes receptors for IL-2β, IL-3, IL-4, IL-6, IL-7, growth hormone, and erythropoietin. Prolactin can influence the immune system through the thymus, inducing IL-2 receptors on lymphocytes. Lymphocytes synthesize and release a biologically active form of prolactin that acts as an autocrine and paracrine growth factor. Treatment with corticosteroids can suppress production of prolactin, leading to the hypothesis that reduction of circulating prolactin accounts for some of the immunosuppressive actions of this class of drugs. Dexamethasone decreases circulating prolactin and inhibits gene expression of both pituitary prolactin and lymphocyte prolactin.
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This chapter discusses estrogen and prolactin and its contributions to autoimmunity in murine models of systemic lupus erythematosus (SLE). It discusses the immunostimulating properties of estrogen and prolactin in murine models, as well as the interactions between estrogen and prolactin, in the context of treating the autoimmune illness, (SLE). Estrogen has powerful effects on the immune system through mechanisms that are regulated differently through two types of estrogen receptors. Immunostimulatory effects of estrogen are expressed in B-cells in BALB/c mice, which have a genetic background that predisposes to loss of B-cell tolerance. The observation that estrogen can stimulate the immune system led to an attempt to control auto-immune disease with diet. The lesions were completely absent if the mice were fed a diet with normal levels of phyto-estrogen. Estrogen and prolactin both play important roles in stimulating the autoimmune disease, SLE. In experimental models of lupus, either hormone is capable of augmenting autoimmunity. When the effects of very high doses of estrogen were tested in mice, experimental results were obscured by estrogen toxicity, which led to early death from causesunrelated to autoimmune disease.
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Prolactin (PRL) has the potential to stimulate immune responses and is a cytokine. Circulating PRL is elevated above the norm in a number of autoimmune diseases, including systemic lupus erythematosus (SLE). Bromocriptine, which suppresses the pituitary secretion of PRL, has been used with success to treat autoimmune illness. Successful use of PRL-suppressive treatments in selected diseases supports the contention that PRL contributes to active autoimmunity and opens up the possibility of using these relatively nontoxic drugs as adjunct therapy for immune-mediated diseases.
Unproven and experimental therapies
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^☆: Supported by USPHS grants NS17423 and NS22512.

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Potentiation of antibody responsiveness after the transplantation of a syngeneic pituitary gland☆

Abstract

Life Sci.

Brain Res.

J. Neurol. Sci.

Cell. Immunol.

Immunopharmacology

The anterior pituitary-grafted rat: a valid model of chronic hyperprolactinemia

Endocr. Rev.

Specific binding of growth hormone to thymocytes

Nature

Gonadotropins and sex hormones

Prolactin and other lactogenic hormones

Suppression of macrophage activation and T-lymphocyte function in hyperprolactinemic mice

Science

Characteristics of immunocompetent cells in the mouse thymus and cell population changes during cortisone-induced atrophy and subsequent regeneration

Cell. Immunol.

Galactorrhea-amenorrhea, bromocryptine and the dopamine receptor

New Engl. J. Med.

Neuroimmunomodulation: neural anatomical basis for impairment and facilitation

Ann. Neurol.

Hypothalamic-immune interactions: neuromodulation of natural killer cell activity by lesioning of the anterior hypothalamus

Immunology