Immunomodulation by bromocriptine

Nagy, Éva; Berczi, István; Wren, Graham E.; Sylvia, L.; Kovács, Kálmán

doi:10.1016/0162-3109(83)90023-1

Cited by 219 publications

(72 citation statements)

References 21 publications

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“…It may also reflect differences in the dose of bromocriptine used or the species and sex of the experimental animals. However, as also reported by Nagy et al (14), bromocriptine alone did decrease antibody production in the present study. Berczi et al showed a marked effect of bromocriptine in the adjuvant arthritis model in female rats (5), but did not investigate male rats.…”

Section: Discussioncontrasting

confidence: 37%

“…Both antibody production (3) and skin test responses to a T cell antigen (4) are decreased by hypophysectomy and can be restored with replacement of prolactin alone. A parallel effect on antibody synthesis or cell mediated immunity is observed after treatment with bromocriptine (14), an ergot-derived dopamine agonist that will markedly inhibit prolactin secretion in doses such as those used in this study. Similarly, the adjuvant-induced arthritis model is significantly inhibited by hypophysectomy or bromocriptine therapy (5).…”

Section: Discussionmentioning

confidence: 86%

“…Similarly, the adjuvant-induced arthritis model is significantly inhibited by hypophysectomy or bromocriptine therapy (5). Another autoimmune model, experimental allergic encephalitis, was also studied demonstrating a marginally significant decrease in the severity of this disease model following bromocriptine therapy (14). Bromocriptine has also been re- some aspects of the immune system.…”

Section: Discussionmentioning

confidence: 99%

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Bromocriptine and low dose cyclosporine in the treatment of experimental autoimmune uveitis in the rat.

Palestine¹,

Muellenberg-Coulombre²,

Kim³

et al. 1987

J. Clin. Invest.

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The immunologic effects of bromocriptine and low dose cyclosporine on experimental autoimmune uveitis (EAU) induced in Lewis rats by S-antigen immunization were studied. Rats treated with a sub-optimal dose (low dose) of cyclosporine (2 mg/kg per d), bromocriptine (1.8 mg/kg per d), or both drugs were compared with untreated rats in regard to the development of EAU, lymphocyte proliferative responses, and anti-S-antigen serum antibodies. Bromocriptine alone decreased the incidence of EAU only in female rats (P < 0.01), did not effect the lymphocyte proliferative response, but did significantly decrease antibody titers in both males (P < 0.004) and females (P < 0.0005). Low dose cyclosporine also partially decreased the incidence of EAU in female rats, but did not decrease antibody titers or lymphocyte proliferative responses. Bromocriptine plus low-dose cyclosporine led to more marked decreases in the incidence of EAU and anti-S-antigen antibody titers as well as in the lymphocyte proliferative assay (P < 0.01 for males, P < 0.0005 for females). This study suggests that bromocriptine can enhance the immunosuppression of low dose cyclosporine.

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Section: Discussioncontrasting

confidence: 37%

Section: Discussionmentioning

confidence: 86%

Section: Discussionmentioning

confidence: 99%

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Bromocriptine and low dose cyclosporine in the treatment of experimental autoimmune uveitis in the rat.

Palestine¹,

Muellenberg-Coulombre²,

Kim³

et al. 1987

J. Clin. Invest.

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“…One difficulty in addressing these issues has been the lack of an appropriate animal model for assessing PRL function. There have been three approaches to studying the effects of PRL deficiency in animals: surgical hypophysectomy (Bates et al, 1962), pharmacological inhibition of PRL secretion (Nagy et al, 1983) and analysis of pituitary dwarf models (Murphy et al, 1992). None of these approaches has been com-pletely satisfactory, for two reasons.…”

Section: Discussionmentioning

confidence: 99%

Defective mammopoiesis, but normal hematopoiesis, in mice with a targeted disruption of the prolactin gene

et al. 1997

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Prolactin (PRL) has been implicated in numerous physiological and developmental processes. The mouse PRL gene was disrupted by homologous recombination. The mutation caused infertility in female mice, but did not prevent female mice from manifesting spontaneous maternal behaviors. PRL-deficient males were fertile and produced offspring with normal Mendelian gender and genotype ratios when they were mated with heterozygous females. Mammary glands of mutant female mice developed a normal ductal tree, but the ducts failed to develop lobular decorations, which is a characteristic of the normal virgin adult mammary gland. The potential effect of PRL gene disruption on antigenindependent primary hematopoiesis was assessed. The results of this analysis indicated that myelopoiesis and primary lymphopoiesis were unaltered in the mutant mice. Consistent with these observations in PRL mutant mice, PRL failed to correct the bone marrow B cell deficiency of Snell dwarf mice. These results argue that PRL does not play any indispensable role in primary lymphocyte development and homeostasis, or in myeloid differentiation. The PRL -/-mouse model provides a new research tool with which to resolve a variety of questions regarding the involvement of both endocrine and paracrine sources of PRL in reproduction, lactogenesis, tumorigenesis and immunoregulation.

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“…Similar to other ILs, PRL acts as a necessary co-mitogen during lymphoid expansion. An immunomodulatory role for PRL was first identified in avian and murine species, secondary to in vivo manipulation of serum PRL levels (Berczi et al 1981, Nagy et al 1983, Glick 1984, Nagy & Berczi 1991. Subsequent in vitro studies have found that in the presence of antigen and/or mitogen, PRL acts as a necessary co-mitogen for T and B cells of human or murine origin (Russell et al 1984, Bernton et al 1988, Hartmann et al 1989, Clevenger et al 1990, Skwarlo-Sonta 1990.…”

Section: Role As a Mitogenmentioning

confidence: 99%