Depletion of eosinophils in mice through the use of antibodies specific for C-C chemokine receptor 3 (CCR3)

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 deplete...

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Veröffentlicht in:Journal of leukocyte biology 1999-06, Vol.65 (6), p.846-853
Hauptverfasser: Grimaldi, J. Christopher, Yu, Nai‐Xuan, 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.
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container_end_page 853
container_issue 6
container_start_page 846
container_title Journal of leukocyte biology
container_volume 65
creator Grimaldi, J. Christopher
Yu, Nai‐Xuan
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.
description 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.
doi_str_mv 10.1002/jlb.65.6.846
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Christopher ; Yu, Nai‐Xuan ; 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.</creator><creatorcontrib>Grimaldi, J. Christopher ; Yu, Nai‐Xuan ; 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.</creatorcontrib><description>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. 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Christopher</creatorcontrib><creatorcontrib>Yu, Nai‐Xuan</creatorcontrib><creatorcontrib>Grunig, Gabrielle</creatorcontrib><creatorcontrib>Seymour, Brian W. P.</creatorcontrib><creatorcontrib>Cottrez, Françoise</creatorcontrib><creatorcontrib>Robinson, Douglas S.</creatorcontrib><creatorcontrib>Hosken, Nancy</creatorcontrib><creatorcontrib>Ferlin, Walter G.</creatorcontrib><creatorcontrib>Wu, Xiaoyan</creatorcontrib><creatorcontrib>Soto, Hortensia</creatorcontrib><creatorcontrib>O'Garra, Anne</creatorcontrib><creatorcontrib>Howard, Maureen C.</creatorcontrib><creatorcontrib>Coffman, Robert L.</creatorcontrib><title>Depletion of eosinophils in mice through the use of antibodies specific for C-C chemokine receptor 3 (CCR3)</title><title>Journal of leukocyte biology</title><addtitle>J Leukoc Biol</addtitle><description>We have generated rat monoclonal antibodies specific for the mouse eotaxin receptor, C‐C chemokine receptor 3 (CCR3). 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P. ; Cottrez, Françoise ; Robinson, Douglas S. ; Hosken, Nancy ; Ferlin, Walter G. ; Wu, Xiaoyan ; Soto, Hortensia ; O'Garra, Anne ; Howard, Maureen C. ; Coffman, Robert L.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4946-3b831f71126945f9ef3898fd3a57978aef6547b1d92c16125f6d43c0c5fb433b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1999</creationdate><topic>3T3 Cells</topic><topic>AIDS/HIV</topic><topic>Animals</topic><topic>Antibodies, Monoclonal - immunology</topic><topic>Antibodies, Monoclonal - pharmacology</topic><topic>Antibody Formation</topic><topic>Antibody Specificity</topic><topic>Bronchoalveolar Lavage Fluid - parasitology</topic><topic>Disease Models, Animal</topic><topic>DNA, Complementary - biosynthesis</topic><topic>Eosinophils - cytology</topic><topic>Epitope Mapping</topic><topic>FACS</topic><topic>Humans</topic><topic>Leukocyte Count - drug effects</topic><topic>Lung - parasitology</topic><topic>Mice</topic><topic>Molecular Sequence Data</topic><topic>Nippostrongylus</topic><topic>Rats</topic><topic>Receptors, CCR3</topic><topic>Receptors, Chemokine - genetics</topic><topic>Receptors, Chemokine - immunology</topic><topic>rodent</topic><topic>Strongylida Infections</topic><topic>Th1</topic><topic>Th2</topic><topic>Th2 Cells - immunology</topic><topic>Tumor Cells, Cultured</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Grimaldi, J. 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Christopher</au><au>Yu, Nai‐Xuan</au><au>Grunig, Gabrielle</au><au>Seymour, Brian W. P.</au><au>Cottrez, Françoise</au><au>Robinson, Douglas S.</au><au>Hosken, Nancy</au><au>Ferlin, Walter G.</au><au>Wu, Xiaoyan</au><au>Soto, Hortensia</au><au>O'Garra, Anne</au><au>Howard, Maureen C.</au><au>Coffman, Robert L.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Depletion of eosinophils in mice through the use of antibodies specific for C-C chemokine receptor 3 (CCR3)</atitle><jtitle>Journal of leukocyte biology</jtitle><addtitle>J Leukoc Biol</addtitle><date>1999-06</date><risdate>1999</risdate><volume>65</volume><issue>6</issue><spage>846</spage><epage>853</epage><pages>846-853</pages><issn>0741-5400</issn><eissn>1938-3673</eissn><abstract>We have generated rat monoclonal antibodies specific for the mouse eotaxin receptor, C‐C chemokine receptor 3 (CCR3). 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source Oxford University Press Journals All Titles (1996-Current); MEDLINE; Wiley Online Library Journals Frontfile Complete; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals
subjects 3T3 Cells
AIDS/HIV
Animals
Antibodies, Monoclonal - immunology
Antibodies, Monoclonal - pharmacology
Antibody Formation
Antibody Specificity
Bronchoalveolar Lavage Fluid - parasitology
Disease Models, Animal
DNA, Complementary - biosynthesis
Eosinophils - cytology
Epitope Mapping
FACS
Humans
Leukocyte Count - drug effects
Lung - parasitology
Mice
Molecular Sequence Data
Nippostrongylus
Rats
Receptors, CCR3
Receptors, Chemokine - genetics
Receptors, Chemokine - immunology
rodent
Strongylida Infections
Th1
Th2
Th2 Cells - immunology
Tumor Cells, Cultured
title Depletion of eosinophils in mice through the use of antibodies specific for C-C chemokine receptor 3 (CCR3)
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