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

  1. Author:
    Chen, K. Q.
    Le, Y. Y.
    Liu, Y.
    Gong, W. H.
    Ying, G. G.
    Huang, J.
    Yoshimura, T.
    Tessarollo, L.
    Wang, J. M.
  2. Author Address

    [Chen, Keqiang; Liu, Ying; Huang, Jian; Yoshimura, Teizo; Wang, Ji Ming] NCI, Mol Immunoregulat Lab, Canc & Inflammat Program, Frederick, MD 21702 USA. [Tessarollo, Lino] NCI, Mouse Canc Genet Program, Ctr Canc Res, Frederick, MD 21702 USA. [Gong, Wanghua] Sci Applicat Int Corp, Frederick, MD 21702 USA. [Chen, Keqiang] Shanghai Jiao Tong Univ, Sch Agr & Biol, Shanghai, Peoples R China. [Le, Yingying] Chinese Acad Sci, Shanghai Inst Biol Sci, Inst Nutr Sci, Shanghai, Peoples R China. [Ying, Guoguang] Tianjin Med Univ, Canc Res Inst & Hosp, Tianjin, Peoples R China.;Wang, JM, NCI, Mol Immunoregulat Lab, Canc & Inflammat Program, Bldg 560,Room 31-76, Frederick, MD 21702 USA.;wangji@mail.nih.gov
    1. Year: 2010
    2. Date: Apr
    3. Epub Date: 3/5/2010
  1. Journal: Journal of Immunology
    1. 184
    2. 7
    3. Pages: 3331-3335
  2. Type of Article: Article
  3. ISSN: 0022-1767
  1. Abstract:

    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.

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External Sources

  1. DOI: 10.4049/jimmunol.0903022
  2. PMID: 20200280
  3. WOS: 000275927600006

Library Notes

  1. Fiscal Year: FY2009-2010
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