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Depletion of eosinophils in mice through the use of antibodies specific for C‐C chemokine receptor 3 (CCR3)
Author(s) -
Grimaldi J. Christopher,
Yu NaiXuan,
Grunig Gabrielle,
Seymour Brian W. P.,
Cottrez Françoise,
Robinson Douglas S.,
Hosken Nancy,
Ferlin Walter G.,
Wu Xiaoyan,
Soto Hortensia,
O'Garra Anne,
Howard Maureen C.,
Coffman Robert L.
Publication year - 1999
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1002/jlb.65.6.846
Subject(s) - ccr3 , cc chemokine receptors , biology , eosinophil , microbiology and biotechnology , monoclonal antibody , chemokine receptor , chemokine , eotaxin , immunology , antibody , immune system , asthma
Abstract We have generated rat monoclonal antibodies specific for the mouse eotaxin receptor, C‐C chemokine receptor 3 (CCR3). Several anti‐CCR3 mAbs proved to be useful for in vivo depletion of CCR3‐expressing cells and immunofluorescent staining. In vivo CCR3 mAbs of the IgG2b isotype substantially depleted blood eosinophil levels in Nippostrongyus brasiliensis ‐infected mice. Repeated anti‐CCR3 mAb treatment in these mice significantly reduced tissue eosinophilia in the lung tissue and bronchoalveolar lavage fluid. Flow cytometry revealed that mCCR3 was expressed on eosinophils but not on stem cells, dendritic cells, or cells from the thymus, lymph node, or spleen of normal mice. Unlike human Th2 cells, mouse Th2 cells did not express detectable levels of CCR3 nor did they give a measurable response to eotaxin. None of the mAbs were antagonists or agonists of CCR3 calcium mobilization. To our knowledge, the antibodies described here are the first mAbs reported to be specific for mouse eosinophils and to be readily applicable for the detection, isolation, and in vivo depletion of eosinophils. J. Leukoc. Biol. 65: 846–853; 1999.