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Cited by 130Asthma and respiratory diseasesChemokine receptors and signalingAllergic Rhinitis and Sensitization

The DOI matches its Crossref record; 38 of the 38 references it cites were found in a registry or an index.

Contribution of CCR4 and CCR8 to antigen-specific TH2 cell trafficking in allergic pulmonary inflammation

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Mikhak, Zamaneh, Fukui, Mieko, Farsidjani, Alireza, Medoff, Benjamin D., Tager, Andrew M., Luster, Andrew D.·2009·Journal of Allergy and Clinical Immunology
DOI 10.1016/j.jaci.2008.09.049PMC PMC2782398
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Abstract

Background Recruitment of antigen-specific T(H)2 cells into the lung is critical for the development of allergic airway inflammation. Although CCR4 and CCR8 are preferentially expressed on T(H)2 cells and CCR4, CCR8, and CXCR3 ligands are increased in asthma, the specific relative contribution of these receptors to antigen-specific T(H)2 cell trafficking into the allergic lung is not known. Objective To determine the relative contribution of the chemokine receptors CCR4, CCR8, and CXCR3 to antigen-specific T(H)2 cell trafficking in a murine model of allergic pulmonary inflammation. Methods We used adoptive transfer experiments to compare the trafficking of wild-type antigen-specific T(H)2 cells with antigen-specific T(H)2 cells deficient in CCR4, CCR8, or CXCR3. Results CCR4-deficient antigen-specific T(H)2 cells failed to traffic efficiently into the lung and the airways. In contrast, CCR8-deficient antigen-specific T(H)2 cells accumulated in these sites. Trafficking of CXCR3-deficient antigen-specific T(H)2 cells and CCR4-deficient and CCR8-deficient antigen-specific T(H)1 cells were comparable to their wild-type counterparts. Approximately 60% of IL-4-producing antigen-specific T cells expressed CCR4. Disruption of CCR4-mediated antigen-specific T(H)2 cell trafficking decreased the levels of T(H)2-type cytokines in the airways and reduced airway eosinophilia and mucus production. Conclusions Our study demonstrates that CCR4 is required for the efficient entry of antigen-specific T(H)2 cells into the lung and the airways in a murine model of allergic pulmonary inflammation.

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Metadata

Authors
Mikhak, Z., Fukui, M., Farsidjani, A., Medoff, B. D., Tager, A. M., & Luster, A. D.
Affiliations
Harvard University (US)
ORCID
Venue
Journal of Allergy and Clinical Immunology
Publisher
Elsevier BV
Published
2009-01
Volume
123
Issue
1
Pages
67-73.e3
ISSN
0091-6749 (ISSN-L)
DOI
10.1016/j.jaci.2008.09.049
PMC
PMC2782398
OpenAlex
W2043133666
Cited by
127
References
38
Citations by year
2026: 2 · 2025: 6 · 2024: 7 · 2023: 5 · 2022: 8 · 2021: 12 · 2020: 7 · 2019: 4 · 2018: 3 · 2017: 3 · 2016: 4 · 2015: 8 · 2014: 10 · 2013: 12 · 2012: 11
FWCI
5.33
Type
journal article
Language
en
Open access
Licence
Locations
  • Journal of Allergy and Clinical Immunology (publishedVersion)
  • PubMed (publishedVersion)
  • PubMed Central (acceptedVersion)
Funders
National Institute of Allergy and Infectious Diseases (R01AI040618, K08AI067519, R37AI040618)
Topics
  • Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Asthma and respiratory diseases
  • Health Sciences › Medicine › Oncology › Chemokine receptors and signaling
  • Health Sciences › Medicine › Immunology and Allergy › Allergic Rhinitis and Sensitization
Keywords
CCR4, CCR8, CXCR3, Th2 cells, allergic airway inflammation, asthma, chemokine receptors, IL-4, airway eosinophilia, mucus production, adoptive transfer
MeSH terms
Animals, Antigens, Cell Movement, Disease Models, Animal, Lung, Pneumonia, Respiratory Hypersensitivity, Mice, Knockout, Th1 Cells, Th2 Cells, Mice, Receptors, CXCR3, Receptors, CCR4, Receptors, CCR8

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