CD11b immunophenotyping identifies inflammatory profiles in the mouse and human lungs.
CD11b immunophenotyping identifies inflammatory profiles in the mouse and human lungs.
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DOI:
10.1038/mi.2015.84
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发表时间:
2016-03
影响因子:
8
通讯作者:
Hibbs ML
中科院分区:
文献类型:
--
作者:
Duan M;Steinfort DP;Smallwood D;Hew M;Chen W;Ernst M;Irving LB;Anderson GP;Hibbs ML
The development of easily accessible tools for human immunophenotyping to classify patients into discrete disease endotypes is advancing personalized therapy. However, no systematic approach has been developed for the study of inflammatory lung diseases with often complex and highly heterogeneous disease etiologies. We have devised an internally standardized flow cytometry approach that can identify parallel inflammatory alveolar macrophage phenotypes in both the mouse and human lungs. In mice, lung innate immune cell alterations during endotoxin challenge, influenza virus infection, and in two genetic models of chronic obstructive lung disease could be segregated based on the presence or absence of CD11b alveolar macrophage upregulation and lung eosinophilia. Additionally, heightened alveolar macrophage CD11b expression was a novel feature of acute lung exacerbations in the SHIP-1−/− model of chronic obstructive lung disease, and anti-CD11b antibody administration selectively blocked inflammatory CD11bpos but not homeostatic CD11bneg alveolar macrophages in vivo. The identification of analogous profiles in respiratory disease patients highlights this approach as a translational avenue for lung disease endotyping and suggests that heterogeneous innate immune cell phenotypes are an underappreciated component of the human lung disease microenvironment. The online version of this article (doi:10.1038/mi.2015.84) contains supplementary material, which is available to authorized users.
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DOI:
10.1084/jem.20020873
发表时间:
2002-09-02
期刊:
The Journal of experimental medicine
影响因子:
--
作者:
Ernst M;Inglese M;Scholz GM;Harder KW;Clay FJ;Bozinovski S;Waring P;Darwiche R;Kay T;Sly P;Collins R;Turner D;Hibbs ML;Anderson GP;Dunn AR
通讯作者:
Dunn AR
影响因子:
6.4
作者:
Gloria Sans-Fons, M.;Yeramian, Andree;Celada, Antonio
通讯作者:
Celada, Antonio
影响因子:
30.5
作者:
通讯作者:
--
影响因子:
4.4
作者:
Maxwell, Mhairi J.;Duan, Mubing;Hibbs, Margaret L.
通讯作者:
Hibbs, Margaret L.
影响因子:
20.3
作者:
Ghia, P;Guida, G;Caligaris-Cappio, F
通讯作者:
Caligaris-Cappio, F