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生长抑素受体在小鼠脾脏及派尔集合淋巴结T淋巴细胞和B淋巴细胞上的分布

Distribution of somatostatin receptors on murine spleen and Peyer's patch T and B lymphocytes.

作者信息

Scicchitano R, Dazin P, Bienenstock J, Payan D G, Stanisz A M

机构信息

Department of Pathology, McMaster University, Hamilton, Ontario, Canada.

出版信息

Brain Behav Immun. 1987 Jun;1(2):173-84. doi: 10.1016/0889-1591(87)90019-5.

Abstract

Recent evidence suggests that the neuropeptide somatostatin (SOM) plays an immunoregulatory role. We demonstrated previously that SOM inhibits concanavalin A-induced cell proliferation and immunoglobulin synthesis by murine Peyer's patch and splenic lymphocytes. Available data suggest that these effects are in part mediated by specific SOM receptors expressed by lymphocytes, but as yet these receptors have not been characterized. Using cytofluorimetry we investigated the distribution and specificity of binding of fluorescent SOM (SOM*) to murine Peyer's patch and splenic T- and B-lymphocyte subpopulations. The specificity of binding was confirmed by radioassay. T and B cells from both organs showed specific binding of SOM*. In Peyer's patches, approximately 50% of all cell populations studied (whole, T- and B-cell-enriched) bound SOM specifically and this was significantly higher than the corresponding splenic lymphocyte populations. Eighty to eighty-four percent of Peyer's patch Thy1.2+, Lyt1+, or L3T4+ cells and 94% of Lyt2+ cells bound SOM. Greater than 80% of B cells from this organ bound SOM (sIgA+ = sIgM+ greater than sIgG+ cells). In spleen, approximately 30% of Thy1.2+, Lyt1+, or L3T4+ cells bound SOM and this was significantly less than the proportion of Lyt2+ cells (53%) which did so. More sIgA+ (89%) than sIgG+ (66%) than sIgM+ (55%) B cells bound SOM*. Although we have previously shown that the effect of SOM on immunoglobulin synthesis was relatively isotype-specific (IgA synthesis was predominantly affected, especially in Peyer's patches) this cannot be explained solely on the basis of preferential expression of SOM receptors by distinct lymphocyte subsets. Instead, it is probably the result of the specific immunological microenvironment in which the lymphocytes reside.

摘要

最近的证据表明,神经肽生长抑素(SOM)发挥免疫调节作用。我们之前证明,SOM可抑制伴刀豆球蛋白A诱导的小鼠派伊尔结和脾淋巴细胞的细胞增殖及免疫球蛋白合成。现有数据表明,这些效应部分是由淋巴细胞表达的特异性SOM受体介导的,但这些受体尚未得到鉴定。我们使用细胞荧光测定法研究了荧光SOM(SOM*)与小鼠派伊尔结及脾T淋巴细胞和B淋巴细胞亚群结合的分布及特异性。通过放射分析证实了结合的特异性。来自这两个器官的T细胞和B细胞均显示出SOM的特异性结合。在派伊尔结中,所研究的所有细胞群体(全细胞、富集T细胞和B细胞的群体)中约50%特异性结合SOM,这显著高于相应的脾淋巴细胞群体。派伊尔结中80%至84%的Thy1.2+、Lyt1+或L3T4+细胞以及94%的Lyt2+细胞结合SOM。该器官中超过80%的B细胞结合SOM(sIgA+ = sIgM+ > sIgG+细胞)。在脾脏中,约30%的Thy1.2+、Lyt1+或L3T4+细胞结合SOM,这显著低于结合SOM的Lyt2+细胞比例(53%)。结合SOM的B细胞中,sIgA+(89%)多于sIgG+(66%)多于sIgM+(55%)。尽管我们之前表明SOM对免疫球蛋白合成的影响相对具有同种型特异性(IgA合成受影响最显著,尤其是在派伊尔结中),但这不能仅基于不同淋巴细胞亚群对SOM受体的优先表达来解释。相反,这可能是淋巴细胞所处的特定免疫微环境的结果。

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