T cells and ILC2s are major effector cells in influenza-induced exacerbation of allergic airway inflammation in mice.
T cells and ILC2s are major effector cells in influenza-induced exacerbation of allergic airway inflammation in mice.
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DOI:
10.1002/eji.201747421
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发表时间:
2019-01
影响因子:
5.4
通讯作者:
Hendriks RW
中科院分区:
文献类型:
--
作者:
Li BWS;de Bruijn MJW;Lukkes M;van Nimwegen M;Bergen IM;KleinJan A;GeurtsvanKessel CH;Andeweg A;Rimmelzwaan GF;Hendriks RW
Influenza virus infection is an important cause of severe asthma exacerbations, but it remains unclear how a Th1‐mediated antiviral response triggers a prototypical Th2 disease. We investigated CD4+ T cells and group 2 innate lymphoid cells (ILC2s) in influenza virus‐infected mice. We found that ILC2s accumulated in the lung rapidly after influenza virus infection, but the induction of IL‐5 and IL‐13 secretion was delayed and concomitant with T cell activation. In an influenza‐induced exacerbation of allergic airway inflammation model we noticed an initial reduction of ILC2 numbers and cytokine production in broncho‐alveolar lavage compared to chronic house dust mite (HDM)‐mediated airway inflammation alone. ILC2s phenotype was characterized by low T1/ST2, ICOS, KLRG1, and CD25 expression, resembling naïve ILC2s. The contribution of ILC2s to type 2 cytokine production in the early stage of the influenza‐induced exacerbation was limited. In contrast, T cells showed increased IL‐4 and IL‐5 production when exposed to both HDM and influenza virus. Upon virus clearance, ILC2s regained an activated T1/ST2highICOShighKLRG1highCD25high phenotype paired with cytokine production and were major contributors to the type 2 cytokine milieu. Collectively, our data indicate that both T cells and ILC2s contribute to influenza‐induced exacerbation of allergic airway inflammation, but with different kinetics.
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DOI:
10.1084/jem.20090410
发表时间:
2009-10-26
期刊:
The Journal of experimental medicine
影响因子:
--
作者:
GeurtsvanKessel CH;Willart MA;Bergen IM;van Rijt LS;Muskens F;Elewaut D;Osterhaus AD;Hendriks R;Rimmelzwaan GF;Lambrecht BN
通讯作者:
Lambrecht BN
影响因子:
6.7
作者:
Gorski SA;Hahn YS;Braciale TJ
通讯作者:
Braciale TJ
DOI:
10.4049/jimmunol.1101632
发表时间:
2012-03-15
期刊:
Journal of immunology (Baltimore, Md. : 1950)
影响因子:
--
作者:
Doherty TA;Khorram N;Sugimoto K;Sheppard D;Rosenthal P;Cho JY;Pham A;Miller M;Croft M;Broide DH
通讯作者:
Broide DH
影响因子:
32.4
作者:
Halim, Timotheus Y. F.;Krauss, Ramona H.;Takei, Fumio
通讯作者:
Takei, Fumio
影响因子:
24.3
作者:
Chung, Kian Fan;Wenzel, Sally E.;Teague, W. Gerald
通讯作者:
Teague, W. Gerald