title: Cutting edge: STAT6 signaling in eosinophils is necessary for development of allergic airway inflammation.
abstract: Eosinophils are critical cellular mediators in allergic asthma and inflammation; however, the signals that regulate their functions are unclear. The transcription factor STAT6 regulates Th2 cytokine responses, acting downstream of IL-4 and IL-13. We showed previously that eosinophil-derived IL-13 plays an important role in the recruitment of T cells to the lung and the subsequent development of allergic asthma. However, whether eosinophils respond to Th2 signals to control allergic airway inflammation is unclear. In this report, we show that STAT6(-/-) eosinophils are unable to induce the development of allergic lung inflammation, including recruitment of CD4(+) T cells, mucus production, and development of airways hyperresponsiveness. This is likely due to the reduced migration of STAT6(-/-) eosinophils to the lung and in response to eotaxin. These data indicate that, like Th cells, eosinophils need to respond to Th2 cytokines via STAT6 during the development of allergic airway inflammation.
authors: Pathobiology Graduate Program, Center for Molecular Immunology and Infectious Diseases, Department of Veterinary and Biomedical Sciences, The Pennsylvania State University, University Park, PA 16802; and Department of Microbiology and Immunology, Cornell University, Ithaca, NY 14853.
authors: Kindra
authors: K
authors: Stokes
authors: Department of Microbiology and Immunology, Cornell University, Ithaca, NY 14853.
authors: Nelson M
authors: NM
authors: LaMarche
authors: Department of Microbiology and Immunology, Cornell University, Ithaca, NY 14853.
authors: Nasif
authors: N
authors: Islam
authors: Department of Microbiology and Immunology, Cornell University, Ithaca, NY 14853.
authors: Amie
authors: A
authors: Wood
authors: Department of Microbiology and Immunology, Cornell University, Ithaca, NY 14853.
authors: Weishan
authors: http://orcid.org/0000-0002-1330-1131
authors: W
authors: Huang
authors: Department of Microbiology and Immunology, Cornell University, Ithaca, NY 14853 averyaugust@cornell.edu.
authors: Avery
authors: http://orcid.org/0000-0003-4968-3415
authors: A
authors: August
mesh_terms: D000818:Animals; D001249:Asthma / Q000235:genetics / Q000276:immunology / Q000378:metabolism; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology / Q000378:metabolism; D018414:CD8-Positive T-Lymphocytes / Q000276:immunology / Q000378:metabolism; D002465:Cell Movement / Q000235:genetics / Q000276:immunology; D016207:Cytokines / Q000276:immunology / Q000378:metabolism; D004804:Eosinophils / Q000276:immunology* / Q000378:metabolism; D005434:Flow Cytometry; D007249:Inflammation / Q000235:genetics / Q000276:immunology* / Q000378:metabolism; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D008822:Mice, Transgenic; D010047:Ovalbumin / Q000276:immunology; D012130:Respiratory Hypersensitivity / Q000235:genetics / Q000276:immunology* / Q000378:metabolism; D050800:STAT6 Transcription Factor / Q000235:genetics / Q000276:immunology* / Q000378:metabolism; D015398:Signal Transduction / Q000235:genetics / Q000276:immunology*; D018418:Th2 Cells / Q000276:immunology / Q000378:metabolism
chemical_list: D016207:Cytokines; D050800:STAT6 Transcription Factor; D010047:Ovalbumin