The chemokines are a large group of chemotactic cytokines that regulate leukocyte trafficking and have recently been shown to inhibit human immunodeficiency virus entry into cells. Eotaxin is a C–C chemokine implicated in the recruitment of eosinophils in a variety of inflammatory disorders and, unlike all other eosinophil chemoattractants, is eosinophil specific. However, given the large number of chemoattractants that have activities on eosinophils, it is unclear whether eotaxin has an important role in vivo. Furthermore, it remains unclear why there is constitutive expression of eotaxin in healthy states in the absence of eosinophilic inflammation. To begin to determine the significance of eotaxin at baseline and during eosinophil-mediated disease processes, we have used targeted gene disruption to generate mice that are deficient in eotaxin. Such mice demonstrate that eotaxin enhances the magnitude of the early (but not late) eosinophil recruitment after antigen challenge in models of asthma and stromal keratitis. Surprisingly, a role for eotaxin in regulating the constitutive number of eosinophils in the peripheral circulation is also demonstrated. These results indicate a contributory role for eotaxin in the generation of peripheral blood and antigen-induced tissue eosinophilia.
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17 February 1997
Brief Definitive Report|
February 17 1997
Targeted Disruption of the Chemokine Eotaxin Partially Reduces Antigen-induced Tissue Eosinophilia
Marc E. Rothenberg,
Marc E. Rothenberg
From the *Howard Hughes Medical Institute, Department of Genetics, Harvard Medical School, Boston, Massachusetts 02115; ‡Allergy Unit, §Infectious Disease Unit, Department of Medicine, Massachusetts General Hospital, Boston, Massachusetts 02114; ‖Division of Geographic Medicine, Case Western Reserve University School of Medicine, Cleveland, Ohio 44106
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James A. MacLean,
James A. MacLean
From the *Howard Hughes Medical Institute, Department of Genetics, Harvard Medical School, Boston, Massachusetts 02115; ‡Allergy Unit, §Infectious Disease Unit, Department of Medicine, Massachusetts General Hospital, Boston, Massachusetts 02114; ‖Division of Geographic Medicine, Case Western Reserve University School of Medicine, Cleveland, Ohio 44106
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Eric Pearlman,
Eric Pearlman
From the *Howard Hughes Medical Institute, Department of Genetics, Harvard Medical School, Boston, Massachusetts 02115; ‡Allergy Unit, §Infectious Disease Unit, Department of Medicine, Massachusetts General Hospital, Boston, Massachusetts 02114; ‖Division of Geographic Medicine, Case Western Reserve University School of Medicine, Cleveland, Ohio 44106
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Andrew D. Luster,
Andrew D. Luster
From the *Howard Hughes Medical Institute, Department of Genetics, Harvard Medical School, Boston, Massachusetts 02115; ‡Allergy Unit, §Infectious Disease Unit, Department of Medicine, Massachusetts General Hospital, Boston, Massachusetts 02114; ‖Division of Geographic Medicine, Case Western Reserve University School of Medicine, Cleveland, Ohio 44106
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Philip Leder
Philip Leder
From the *Howard Hughes Medical Institute, Department of Genetics, Harvard Medical School, Boston, Massachusetts 02115; ‡Allergy Unit, §Infectious Disease Unit, Department of Medicine, Massachusetts General Hospital, Boston, Massachusetts 02114; ‖Division of Geographic Medicine, Case Western Reserve University School of Medicine, Cleveland, Ohio 44106
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Marc E. Rothenberg
From the *Howard Hughes Medical Institute, Department of Genetics, Harvard Medical School, Boston, Massachusetts 02115; ‡Allergy Unit, §Infectious Disease Unit, Department of Medicine, Massachusetts General Hospital, Boston, Massachusetts 02114; ‖Division of Geographic Medicine, Case Western Reserve University School of Medicine, Cleveland, Ohio 44106
James A. MacLean
From the *Howard Hughes Medical Institute, Department of Genetics, Harvard Medical School, Boston, Massachusetts 02115; ‡Allergy Unit, §Infectious Disease Unit, Department of Medicine, Massachusetts General Hospital, Boston, Massachusetts 02114; ‖Division of Geographic Medicine, Case Western Reserve University School of Medicine, Cleveland, Ohio 44106
Eric Pearlman
From the *Howard Hughes Medical Institute, Department of Genetics, Harvard Medical School, Boston, Massachusetts 02115; ‡Allergy Unit, §Infectious Disease Unit, Department of Medicine, Massachusetts General Hospital, Boston, Massachusetts 02114; ‖Division of Geographic Medicine, Case Western Reserve University School of Medicine, Cleveland, Ohio 44106
Andrew D. Luster
From the *Howard Hughes Medical Institute, Department of Genetics, Harvard Medical School, Boston, Massachusetts 02115; ‡Allergy Unit, §Infectious Disease Unit, Department of Medicine, Massachusetts General Hospital, Boston, Massachusetts 02114; ‖Division of Geographic Medicine, Case Western Reserve University School of Medicine, Cleveland, Ohio 44106
Philip Leder
From the *Howard Hughes Medical Institute, Department of Genetics, Harvard Medical School, Boston, Massachusetts 02115; ‡Allergy Unit, §Infectious Disease Unit, Department of Medicine, Massachusetts General Hospital, Boston, Massachusetts 02114; ‖Division of Geographic Medicine, Case Western Reserve University School of Medicine, Cleveland, Ohio 44106
Address correspondence to Marc Rothenberg, Department of Pediatrics, 3333 Burnet Avenue, Cincinnati, OH 45229.
Received:
November 27 1996
Revision Received:
December 26 1996
Online ISSN: 1540-9538
Print ISSN: 0022-1007
1997
J Exp Med (1997) 185 (4): 785–790.
Article history
Received:
November 27 1996
Revision Received:
December 26 1996
Citation
Marc E. Rothenberg, James A. MacLean, Eric Pearlman, Andrew D. Luster, Philip Leder; Targeted Disruption of the Chemokine Eotaxin Partially Reduces Antigen-induced Tissue Eosinophilia. J Exp Med 17 February 1997; 185 (4): 785–790. doi: https://doi.org/10.1084/jem.185.4.785
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