Cutting Edge: A Critical Role for the G Protein-Coupled Receptor mFPR2 in Airway Inflammation and Immune Responses

被引：106

作者：

Chen, Keqiang ^{[1
,4
]}

Le, Yingying ^{[5
]}

Liu, Ying ^{[1
]}

Gong, Wanghua ^{[3
]}

Ying, Guoguang ^{[6
]}

Huang, Jian ^{[1
]}

Yoshimura, Teizo ^{[1
]}

Tessarollo, Lino ^{[2
]}

Wang, Ji Ming ^{[1
]}

机构：

[1] NCI, Mol Immunoregulat Lab, Canc & Inflammat Program, Frederick, MD 21702 USA

[2] NCI, Mouse Canc Genet Program, Ctr Canc Res, Frederick, MD 21702 USA

[3] Sci Applicat Int Corp, Frederick, MD 21702 USA

[4] Shanghai Jiao Tong Univ, Sch Agr & Biol, Shanghai, Peoples R China

[5] Chinese Acad Sci, Shanghai Inst Biol Sci, Inst Nutr Sci, Shanghai, Peoples R China

[6] Tianjin Med Univ, Canc Res Inst & Hosp, Tianjin, Peoples R China

来源：

JOURNAL OF IMMUNOLOGY | 2010年 / 184卷 / 07期

基金：

美国国家卫生研究院;

关键词：

N-FORMYLPEPTIDE RECEPTOR; DENDRITIC CELLS; LIPOXIN A(4); PEPTIDE; ACTIVATION; INDUCTION; ANTIGEN; ASTHMA; FPRL2;

D O I：

10.4049/jimmunol.0903022

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

071005 [微生物学]; 100108 [医学免疫学];

摘要：

The formylpeptide receptor-like 1, now officially termed FPR2, in human and its mouse homolog mFPR2 mediate leukocyte migration in response to agonists associated with inflammation and immune responses. To clarify the in vivo role of the receptor, we generated mice deficient in mFPR2. mFPR2(-/-) mice showed markedly reduced severity in OVA/alum-induced allergic airway inflammation. This was associated with diminished recruitment of CD11c(+) dendritic cells into the airway mucosa and secondary lymphoid organs, as well as reduced production of Type 2 cytokines and Igs. We also found that the bronchoalveolar lavage fluid from wild type mice with airway inflammation contained mFPR2 agonist activity. This study reveals a critical role for mFPR2 in the progression of allergic airway inflammation and immune responses. The Journal of Immunology, 2010, 184: 3331-3335.

引用

页码：3331 / 3335

页数：5

共 22 条

[1]

Role of G-protein-coupled signaling in the induction and regulation of dendritic cell function by Toxoplasma gondii [J].