A. M. Coelho-Castelo, A. Panunto-Castelo, Alan Berlese, J. Silva, V. Rodrigues
{"title":"The Mannose-Binding Protein Sm60 from Schistosoma mansoni Suppresses T Cell Proliferation via Inhibition of Interleukin-2 Production","authors":"A. M. Coelho-Castelo, A. Panunto-Castelo, Alan Berlese, J. Silva, V. Rodrigues","doi":"10.2174/1875035401003010001","DOIUrl":null,"url":null,"abstract":"Adult worms of Schistosoma mansoni live in the bloodstream, employing immune evasion strategies and exposing few antigens to the immune system. The tegumental surface of adult worms presents Sm60, a mannose-binding protein, which induces neutrophil migration and mast cell degranulation. Here we demonstrated that Sm60 is able to block the in vitro antigen-specific or polyclonal spleen cell proliferation induced by keyhole limpet haemocyanin (KLH) or con- canavalin A (Con A), respectively. To address the mechanism of inhibition, we evaluated some cytokines in culture and observed that Sm60 decreased significantly the synthesis of interleukin (IL)-2 induced in response to KLH, but not other cytokines. To block the suppression triggered by Sm60, exogenous IL-2 or α-methyl-mannoside were added to KLH- stimulated cultures pulsed with Sm60. Only IL-2 abolished the Sm60 effect, suggesting that Sm60 blocked the lymphop- roliferation through the inhibition of IL-2 production, in a carbohydrate recognition domain (CRD)-independent mecha- nism. Our results suggest that Sm60 could participate in the immune evasion mechanisms of S. mansoni.","PeriodicalId":88763,"journal":{"name":"The open vaccine journal","volume":"3 1","pages":"1-6"},"PeriodicalIF":0.0000,"publicationDate":"2010-01-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"1","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"The open vaccine journal","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.2174/1875035401003010001","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 1
Abstract
Adult worms of Schistosoma mansoni live in the bloodstream, employing immune evasion strategies and exposing few antigens to the immune system. The tegumental surface of adult worms presents Sm60, a mannose-binding protein, which induces neutrophil migration and mast cell degranulation. Here we demonstrated that Sm60 is able to block the in vitro antigen-specific or polyclonal spleen cell proliferation induced by keyhole limpet haemocyanin (KLH) or con- canavalin A (Con A), respectively. To address the mechanism of inhibition, we evaluated some cytokines in culture and observed that Sm60 decreased significantly the synthesis of interleukin (IL)-2 induced in response to KLH, but not other cytokines. To block the suppression triggered by Sm60, exogenous IL-2 or α-methyl-mannoside were added to KLH- stimulated cultures pulsed with Sm60. Only IL-2 abolished the Sm60 effect, suggesting that Sm60 blocked the lymphop- roliferation through the inhibition of IL-2 production, in a carbohydrate recognition domain (CRD)-independent mecha- nism. Our results suggest that Sm60 could participate in the immune evasion mechanisms of S. mansoni.
曼氏血吸虫的成虫生活在血液中,采用免疫逃避策略,并向免疫系统暴露很少的抗原。成虫的被皮表面含有Sm60,一种甘露糖结合蛋白,可诱导中性粒细胞迁移和肥大细胞脱颗粒。在这里,我们证明Sm60能够分别阻断锁孔帽贝血青素(KLH)或con- canavalin A (con A)诱导的体外抗原特异性或多克隆脾细胞增殖。为了解决抑制机制,我们在培养中评估了一些细胞因子,并观察到Sm60显著降低了KLH诱导的白细胞介素(IL)-2的合成,但对其他细胞因子没有影响。为了阻断Sm60引发的抑制,在Sm60脉冲的KLH刺激培养物中加入外源IL-2或α-甲基甘露糖甙。只有IL-2消除了Sm60的作用,这表明Sm60通过抑制IL-2的产生来阻断淋巴细胞的增殖,其机制与碳水化合物识别结构域(CRD)无关。结果提示Sm60可能参与了曼氏梭菌的免疫逃避机制。