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CLC number: R562.2

On-line Access: 2015-07-03

Received: 2014-10-23

Revision Accepted: 2015-02-01

Crosschecked: 2015-06-15

Cited: 2

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Citations:  Bibtex RefMan EndNote GB/T7714


Hui-ying Wang


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Journal of Zhejiang University SCIENCE B 2015 Vol.16 No.7 P.622-631


Anti-CD69 monoclonal antibody treatment inhibits airway inflammation in a mouse model of asthma

Author(s):  Hui-ying Wang, Yu Dai, Jiao-li Wang, Xu-yan Yang, Xin-guo Jiang

Affiliation(s):  Department of Allergy, the Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou 310009, China; more

Corresponding email(s):   marywang@zju.edu.cn

Key Words:  Cluster of differentiation 69 (CD69), Eosinophil, Interleukin-5 (IL-5), Asthma

Hui-ying Wang, Yu Dai, Jiao-li Wang, Xu-yan Yang, Xin-guo Jiang. Anti-CD69 monoclonal antibody treatment inhibits airway inflammation in a mouse model of asthma[J]. Journal of Zhejiang University Science B, 2015, 16(7): 622-631.

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author="Hui-ying Wang, Yu Dai, Jiao-li Wang, Xu-yan Yang, Xin-guo Jiang",
journal="Journal of Zhejiang University Science B",
publisher="Zhejiang University Press & Springer",

%0 Journal Article
%T Anti-CD69 monoclonal antibody treatment inhibits airway inflammation in a mouse model of asthma
%A Hui-ying Wang
%A Yu Dai
%A Jiao-li Wang
%A Xu-yan Yang
%A Xin-guo Jiang
%J Journal of Zhejiang University SCIENCE B
%V 16
%N 7
%P 622-631
%@ 1673-1581
%D 2015
%I Zhejiang University Press & Springer
%DOI 10.1631/jzus.B1400285

T1 - Anti-CD69 monoclonal antibody treatment inhibits airway inflammation in a mouse model of asthma
A1 - Hui-ying Wang
A1 - Yu Dai
A1 - Jiao-li Wang
A1 - Xu-yan Yang
A1 - Xin-guo Jiang
J0 - Journal of Zhejiang University Science B
VL - 16
IS - 7
SP - 622
EP - 631
%@ 1673-1581
Y1 - 2015
PB - Zhejiang University Press & Springer
ER -
DOI - 10.1631/jzus.B1400285

Objective: Airway inflammation and airway hyper-responsiveness (AHR) are principle pathological manifestations of asthma. cluster of differentiation 69 (CD69) is a well-known co-stimulatory factor associated with the activation, proliferation as well as apoptosis of immune cells. This study aims to examine the effect of anti-CD69 monoclonal antibody (mAb) on the pathophysiology of a mouse model of asthma. Methods: A murine model of ovalbumin (OVA)-induced allergic airway inflammation was used in this study. Briefly, mice were injected with 20 μg chicken OVA intraperitoneally on Days 0 and 14, followed by aerosol provocation with 1% (0.01 g/ml) OVA on Days 24, 25, and 26. Anti-CD69 mAb or isotype IgG was injected intraperitoneally after OVA challenge; dexamethasone (DXM) was administrated either before or after OVA challenge. AHR, mucus production, and eosinophil infiltration in the peribronchial area were examined. The levels of granulocyte-macrophage colony-stimulating factor (GM-CSF) and interleukin-5 (IL-5) in bronchoalveolar lavage fluid (BALF) were also assayed as indices of airway inflammation on Day 28 following OVA injection. Results: Pretreatment with DXM together with anti-CD69 mAb treatment after OVA provocation completely inhibited AHR, eosinophil infiltration and mucus overproduction, and significantly reduced BALF IL-5. However, treatment with DXM alone after OVA challenge only partially inhibited AHR, eosinophil infiltration and mucus overproduction, and did not diminish BALF IL-5. Treatment with either DXM or anti-CD69 mAb did not alter the concentration of BALF GM-CSF. Conclusions: Anti-CD69 mAb treatment inhibits established airway inflammation as effectively as DXM pretreatment. This study provides a potential alternative therapeutic opportunity for the clinical management of asthma and its exacerbation.




Darkslateblue:Affiliate; Royal Blue:Author; Turquoise:Article


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