β(2) integrins rather than β(1) integrins mediate Alternaria-induced group 2 innate lymphoid cell trafficking to the lung.
β(2) integrins rather than β(1) integrins mediate Alternaria-induced group 2 innate lymphoid cell trafficking to the lung.
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DOI：
10.1016/j.jaci.2017.03.010
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发表时间：
2018-01
期刊：
影响因子：
--
通讯作者：
Broide DH
中科院分区：
文献类型：
--
作者：
Karta MR;Rosenthal PS;Beppu A;Vuong CY;Miller M;Das S;Kurten RC;Doherty TA;Broide DH
第2组先天淋巴样细胞（ILC2）在由真菌过敏原链格孢菌（Alternaria alternata）诱导的2型炎症期间在小鼠肺中扩增。肺中ILC2数量的增加在很大程度上归因于局部增殖，并且在链格孢属暴露后ILC2是否从循环迁移到肺是未知的。我们检查了人（肺、淋巴结、血液）和小鼠肺ILC2是否表达β1和β2整联蛋白粘附分子，以及这些整联蛋白是否是ILC2运输到小鼠肺中所需的。通过流式细胞术评估人和小鼠ILC2的β1和β2整联蛋白粘附分子的表面表达。通过在小鼠气道暴露于链格孢菌之前体内阻断这些整合素来评估β1和β2整合素在ILC2运输至肺中的作用。人和小鼠肺ILC2均表达高水平的β1和β2整联蛋白粘附受体。链格孢菌攻击的鼻内给药减少了骨髓中的ILC2，同时增加了血液和肺中的ILC2水平。体内阻断β2整合素（CD18）可显著降低肺中ILC2水平，但不改变ILC2增殖、凋亡和功能。相反，体内阻断β1整合素或α4整合素不影响肺ILC2水平。ILC2在小鼠肺中的数量增加不仅通过局部增殖，而且通过使用β2而不是β1或α4整联蛋白从循环运输到肺中。
Group 2 innate lymphoid cells (ILC2s) expand in the lungs of mice during type 2 inflammation induced by the fungal allergen Alternaria alternata. The increase in ILC2 numbers in the lung has been largely attributed to local proliferation and whether ILC2s migrate from the circulation to the lung following Alternaria exposure is unknown. We examined whether human (lung, lymph node, blood) and mouse lung ILC2s express β1 and β2 integrin adhesion molecules, and whether these integrins are required for trafficking of ILC2 into the lungs of mice Human and mouse ILC2s were assessed for surface expression of β1 and β2 integrins adhesion molecules by flow cytometry. The role of β1 and β2 integrins in ILC2 trafficking to the lungs was assessed by in vivo blocking of these integrins prior to airway exposure to Alternaria in mice. Both human and mouse lung ILC2s express high levels of β1 and β2 integrin adhesion receptors. Intranasal administration of Alternaria challenge reduced ILC2s in the bone marrow and concurrently increased blood and lung ILC2 levels. In vivo blocking of β2 integrins (CD18) significantly reduced ILC2 levels in the lungs, but did not alter ILC2 proliferation, apoptosis, and function. In contrast, in vivo blocking of β1 integrins or α4 integrins did not affect lung ILC2 levels. ILC2s increase in number in the mouse lung not only through local proliferation, but also through trafficking from the circulation into the lung using β2 rather than β1 or α4 integrins.
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影响因子：
14.2
作者：
Barlow, Jillian L.;Bellosi, Agustin;McKenzie, Andrew N. J.
通讯作者：
McKenzie, Andrew N. J.
DOI：
10.1016/j.jaci.2014.11.037
发表时间：
2015-07
期刊：
The Journal of allergy and clinical immunology
影响因子：
--
作者：
Christianson CA;Goplen NP;Zafar I;Irvin C;Good JT Jr;Rollins DR;Gorentla B;Liu W;Gorska MM;Chu H;Martin RJ;Alam R
通讯作者：
Alam R
影响因子：
4.4
作者：
Miyazaki, Yasunari;Bunting, Michaeline;Zimmerman, Guy A.
通讯作者：
Zimmerman, Guy A.
影响因子：
16.8
作者：
Di Rosa, F;Pabst, R
通讯作者：
Pabst, R
影响因子：
5.5
作者：
Karta, Maya R.;Broide, David H.;Doherty, Taylor A.
通讯作者：
Doherty, Taylor A.