• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Infection and immunity >Interleukin-12 and tumor necrosis factor alpha mediate innate production of gamma interferon by group B Streptococcus-treated splenocytes of severe combined immunodeficiency mice.
【24h】

Interleukin-12 and tumor necrosis factor alpha mediate innate production of gamma interferon by group B Streptococcus-treated splenocytes of severe combined immunodeficiency mice.

机译：白细胞介素12和肿瘤坏死因子α介导严重的联合免疫缺陷小鼠的B组链球菌治疗的脾细胞先天产生γ干扰素。

获取原文
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

The existence of interleukin-12-mediated innate immune responses to group B streptococci (GBS) was tested by examining T-lymphocyte-independent gamma interferon (IFN) production in cultured splenocytes from severe combined immunodeficiency mice. Splenocytes were cultured with killed or living GBS for 48 h, and then IFN was measured by enzyme-linked immunosorbent assay. Type III GBS as well as other extracellular bacterial agents of neonatal sepsis (staphylococci and enterococci) induced IFN production, which was enhanced by interleukin-2 and was inhibited by neutralizing antibodies to tumor necrosis factor alpha and to mouse interleukin-12. Interleukin-12 bioactivity was present in conditioned medium from GBS-treated adherent macrophages. Adherent peritoneal macrophages and bone marrow-derived natural killer cells from severe combined immunodeficiency mice cultured separately with GBS did not produce IFN, whereas cocultures did produce IFN. Functional macrophage activation was evident by nitric oxide production in GBS-treated splenocyte cultures. The results show that extracellular pathogens such as GBS, similarly to intracellular microbes, induce macrophage interleukin-12 and tumor necrosis factor alpha, which promote natural killer cell secretion of IFN, which then enhances innate phagocyte resistance mechanisms.
机译：通过检查来自严重合并免疫缺陷小鼠的脾细胞中的T淋巴细胞非依赖性γ干扰素（IFN）产生，来测试白介素12介导的对B组链球菌（GBS）的先天免疫反应的存在。用杀死的或存活的GBS培养脾细胞48小时，然后通过酶联免疫吸附测定法测量IFN。 III型GBS以及新生儿败血症的其他细胞外细菌因子（葡萄球菌和肠球菌）诱导IFN产生，白介素2增强了IFN产生，中和抗肿瘤坏死因子α和小鼠白介素12的抗体抑制了IFN的产生。 ILGB-12的生物活性存在于GBS处理的贴壁巨噬细胞的条件培养基中。来自分别与GBS一起培养的严重联合免疫缺陷小鼠的腹膜巨噬细胞和骨髓源性自然杀伤细胞不产生IFN，而共培养则产生IFN。在GBS处理的脾细胞培养物中，一氧化氮的产生可以明显证明功能性巨噬细胞的活化。结果表明，与细胞内微生物类似，细胞外病原体（例如GBS）诱导巨噬细胞白介素12和肿瘤坏死因子α，它们促进IFN的自然杀伤细胞分泌，进而增强先天吞噬细胞的耐药机制。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号