Anterior pituitary hormone control by interleukin 2.

Anterior pituitary hormone control by interleukin 2.
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垂体前叶激素受白介素 2 控制。

DOI:
10.1073/pnas.88.7.2961
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发表时间:
1991
影响因子:
11.1
通讯作者:
McCann,SM
McCann,SM
中科院分区:
综合性期刊1区
文献类型:
--
作者:
Karanth,S;McCann,SM

文献摘要

被引文献

相似文献

几种单核细胞因子,由单核细胞和巨噬细胞分泌的蛋白质,改变垂体前叶激素的释放。我们在这里报告的能力飞摩尔浓度的白细胞介素2(IL-2),T淋巴细胞释放的淋巴因子,直接改变垂体激素的释放。在离体条件下,观察了IL-2浓度在10(-17)~ 10(-9)M范围内对垂体前叶激素释放的影响。将半垂体在1 ml Krebs-Ringer碳酸氢盐缓冲液(KRB)中预孵育,然后与KRB或含有不同浓度IL-2的KRB孵育1或2小时。随后在56 mM钾培养基中孵育30 min,以研究用IL-2预处理对随后去极化诱导的激素释放的影响。通过放射免疫法测定释放到孵育液中的催乳素(PRL)、促黄体生成素(LH)、促卵泡激素(FSH)、促肾上腺皮质激素(ACTH)、生长激素(GH)和促甲状腺激素(TSH)。IL-2刺激基础释放的PRL在1或2小时,但抑制随后的去极化诱导的PRL释放,可能是因为容易释放的PRL池耗尽。最小有效剂量(MED)为10(-15)M。相反,IL-2在1或2小时显著抑制LH和FSH的基础释放,MED为10(-16)M,因此证明了细胞因子对催乳素和促性腺素的相互作用。随后的去极化诱导的LH和FSH的释放被抑制,表明IL-2的持续抑制作用。IL-2在1小时刺激ACTH和TSH释放,MED分别为10(-12)和10(-15)M。相反,IL-2在1小时显著降低GH的基础释放,MED为10(-15)M。GH的释放在2小时时没有改变。高钾诱导的ACTH、TSH和GH的释放没有受到影响。结果表明,IL-2在皮摩尔浓度影响垂体前叶激素的释放。这种细胞因子可以作为淋巴细胞的重要信使,通过从腺体中的淋巴细胞释放或到达腺体的血液中的浓度足以激活它,对垂体产生直接的旁分泌作用。
Several monokines, proteins secreted by monocytes and macrophages, alter release of hormones from the anterior pituitary. We report here the ability of femtomolar concentrations of interleukin 2 (IL-2), a lymphokine released from T lymphocytes, to alter directly pituitary hormone release. The effects of concentrations of IL-2 ranging from 10(-17) to 10(-9) M on anterior pituitary hormone release were evaluated in vitro. Hemipituitaries were preincubated in 1 ml of Krebs-Ringer bicarbonate buffer (KRB) followed by incubation for 1 or 2 hr with KRB or KRB containing different concentrations of IL-2. This was followed by incubation for 30 min in 56 mM potassium medium to study the effect of pretreatment with IL-2 on subsequent depolarization-induced hormone release. Prolactin (PRL), luteinizing hormone (LH), follicle-stimulating hormone (FSH), corticotropin (ACTH), growth hormone (GH), and thyrotropic hormone (TSH) released into the incubation medium were measured by radioimmunoassay. IL-2 stimulated the basal release of PRL at 1 or 2 hr but suppressed the subsequent depolarization-induced PRL release, perhaps because the readily releasable pool of PRL was exhausted. The minimal effective dose (MED) was 10(-15) M. Conversely, IL-2 significantly suppressed the basal release of LH and FSH at 1 or 2 hr, with a MED of 10(-16) M, thus demonstrating a reciprocal action of the cytokine on lactotrophs and gonadotrophs. The subsequent depolarization-induced release of LH and FSH was suppressed, indicative of a persistent inhibitory action of IL-2. IL-2 stimulated ACTH and TSH release at 1 hr and the MEDs were 10(-12) and 10(-15) M, respectively. Conversely, IL-2 significantly lowered the basal release of GH at 1 hr, with a MED of 10(-15) M. The release of GH was not altered at 2 hr. The high potassium-induced release of ACTH, TSH, and GH was not affected. The results demonstrate that IL-2 at picomolar concentrations affects the release of anterior pituitary hormones. This cytokine may serve as an important messenger from lymphocytes exerting a direct paracrine action on the pituitary by its release from lymphocytes in the gland or concentrations in the blood that reach the gland may be sufficient to activate it.