Gabellec M M, Jafarian-Tehrani M, Griffais R, Haour F
Unité de Pharmacologie Neuro-Immuno-Endocrinienne, Institut Pasteur, Paris, France.
Neuroimmunomodulation. 1996 Sep-Oct;3(5):304-9. doi: 10.1159/000097284.
Receptors for IL-1, type I (IL-1R1) and type II (IL-1R2), have been characterized by pharmacological and molecular techniques in the mouse brain. High densities are mainly found in the cortex, dentate gyrus and choroid plexus. It was therefore of interest to investigate the expression of mRNA IL-1 receptor accessory protein (IL-1R AcP), which is a part of the IL-1 receptor complex and has been shown to interact specifically with IL-1R1. IL-1R AcP transcripts were detected under basal conditions following RT-PCR amplification in the mouse brain, as well as in the pituitary, spleen, adrenal and liver. IL-1R AcP transcripts were found in higher amounts than IL-1R1 transcripts in all tissues except the spleen, where their expression was minor. Following bacterial lipopolysaccharide (LPS) stimulation (3-48 h), IL-1R AcP transcripts were not changed in the brain, while IL-1R1 transcripts were increased for 3-6 h. In the spleen, a slight increase in IL-1R AcP and IL-1R1 was observed during the first hours following LPS stimulation. In conclusion, IL-1R AcP mRNA is expressed in the brain and in other tissues where IL-1R1 transcripts are found. However, the regulation of its expression is distinct from IL-1R1. The high level of expression and the lack of regulation of IL-1R AcP transcripts in the brain under inflammatory conditions suggest that the protein might be constitutively expressed in excess.
白细胞介素-1的I型受体(IL-1R1)和II型受体(IL-1R2)已通过药理学和分子技术在小鼠脑中得到鉴定。高密度主要存在于皮质、齿状回和脉络丛中。因此,研究白细胞介素-1受体辅助蛋白(IL-1R AcP)的mRNA表达很有意义,该蛋白是IL-1受体复合物的一部分,已被证明能与IL-1R1特异性相互作用。在小鼠脑以及垂体、脾脏、肾上腺和肝脏中,通过逆转录-聚合酶链反应(RT-PCR)扩增,在基础条件下检测到了IL-1R AcP转录本。除脾脏外,在所有组织中发现的IL-1R AcP转录本数量均高于IL-1R1转录本,脾脏中其表达较少。在细菌脂多糖(LPS)刺激(3 - 48小时)后,脑中的IL-1R AcP转录本没有变化,而IL-1R1转录本在3 - 6小时增加。在脾脏中,LPS刺激后的最初几个小时内观察到IL-1R AcP和IL-1R1略有增加。总之,IL-1R AcP mRNA在脑中以及发现IL-1R1转录本的其他组织中表达。然而,其表达调控与IL-1R1不同。炎症条件下脑中IL-1R AcP转录本的高表达水平和缺乏调控表明该蛋白可能组成性地过量表达。