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Nature：免疫反应如何确定肠道菌群和人体内代谢之间的稳态

2018-01-26 Yui，Michael 转化医学网

免疫系统肠道菌群脂质代谢
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发表在《Nature》上面名为“Innate and adaptive lymphocytes sequentially shape the gut microbiota and lipid metabolism”的文章，为我们揭示了免疫系统如何以不同的形式参与人体肠道菌群和脂质代谢。

发表在《Nature》上面名为“Innate and adaptive lymphocytes sequentially shape the gut microbiota and lipid metabolism”的文章，为我们揭示了免疫系统如何以不同的形式参与人体肠道菌群和脂质代谢。

为了研究微生物环境中原位和适应性免疫细胞的状态和活性，研究人员使用了定量多重性免疫组化。并主要研究具有完整（野生型）或适应性淋巴细胞缺陷（Rag1 - / - ）免疫系统的动物在特定的无病原体条件下远端小肠中磷酸化的STAT3（pSTAT3）存在和分布的情况。

而研究结果显示：STAT3在ILC3和IECs中的磷酸化是由微生物引起的信号传导引起的，而定义的微生物例如SFB在Rag1 - / - 小鼠的这种信号传导中起主要作用。


Rag1 - / - 小鼠小肠微环境诱导的pSTAT3 + ILC3s和IECs

此外，IL-23和IL-22作为功能性连接的细胞因子，分别在ILC3和IECs中具有诱导pSTAT3的潜力。因此通过对pSTAT3的检测，研究人员发现，IL-23和IL-22构成了一个涉及ILC3的通路，并且在缺乏适应性免疫系统的动物的IEC中产生强信号。

虽然这种电路以前曾报道过Rag1缺陷小鼠的病原体感染，但这些新的发现表明，ILC3和IECs在无适应性免疫的情况下被共生菌群牢固地持续激活。


CD4 + T细胞在控制ILC3和IEC激活中的作用

同时，研究还表明在个体发育过程中，先天性淋巴细胞在适应性系统充分发育之前就已经起作用。新出现的适应性反应在很大程度上沉默了ILC反应，并建立了非炎性共栖的稳态。

在缺乏适应性免疫的情况下，大多数细菌（包括SFB）在Rag1 - / - 小鼠中增加。然而，在缺少STAT3激活的情况下，Il23a - / - Rag1 - / - 小鼠的SFB丰度进一步增加。

尽管先天性和适应性淋巴细胞控制了SFB的数量，但扫描电子显微镜显示SFB具有显着不同的形态适应性淋巴细胞存在。在Rag1 - / - 小鼠的回肠中，活化的ILC3s阻止SFB发展成长丝状形式，并且适应性淋巴细胞限制附着于上皮细胞的SFB的数量。

这说明，先天性和适应性淋巴细胞采取不同策略来调节在这些条件，适应性淋巴细胞的活性优于先天性淋巴细胞的活性。

通过对来自共栖野生型，Rag1 - / - 和Tcra - / - 小鼠以及单独饲养的Tcra - / - 小鼠的回肠进行的全组织RNA测序分析及定量实时PCR分析，研究人员发现在缺乏适应性淋巴细胞的情况下，尽管ILC能够抑制微生物群落，但它们的持续活化导致异常的脂质处理和组织内稳态。


在ILC3和IEC激活的小鼠中破坏脂质代谢

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    2018-04-19 liye789132251

    #Nat#

    0

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    2018-04-20 changfy

    #稳态#

    0

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    2018-02-14 yunger

    和我的研究有一定的关系

    0

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    2018-01-31 jyzxjiangqin

    免疫反应的应用.

    0

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    2018-01-28 cnxcy

    #免疫反应#

    0

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    2018-01-28 1249897bm37(暂无昵称)

    #肠道菌#

    0

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    2018-01-26 1e0e5697m83(暂无匿称)

    henhao

    0

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    2018-01-26 changjiu

    学习一下谢谢

    0

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    2018-01-26 清风拂面

    很好的文章谢谢分享

    0

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