title: Suppressors of cytokine signaling 3 expression in eosinophils: regulation by PGE₂ and Th2 cytokines.
abstract: Asthma and nonasthmatic eosinophilic bronchitis (NAEB) are respiratory disorders characterized by a predominance of Th2 cells and eosinophilic inflammation. Suppressors of cytokine signaling (SOCS) proteins play an important role in Th2-mediated allergic responses through control of the balance between Th1 and Th2 cells, particularly, SOCS3 and SOCS5. The aim of this study was to analyze SOCS expression in human peripheral blood eosinophils from patients with asthma, NAEB and healthy controls. SOCS expression in eosinophils from subjects was demonstrated by different techniques. Results showed that expression of SOCS3 in eosinophils and CD4 T cells from patients was higher than in healthy subjects. In addition, we demonstrated that prostaglandin E₂ (PGE₂) and Th2 cytokines are able to upregulate SOCS3 production in eosinophils and attenuate its degranulation. In conclusion, eosinophils are able to transcribe and translate SOCS3 protein and can contribute to the regulation of the Th1/Th2 balance through SOCS3 production.
authors.affiliation: Immunology Department, IIS-Fundación Jiménez Díaz (IIS-FJD), Avenida Reyes Católicos 2, 28040 Madrid, Spain.
authors.forename: Esther
authors.initials: E
authors.lastname: López
authors.forename: María Paz
authors.initials: MP
authors.lastname: Zafra
authors.forename: Beatriz
authors.initials: B
authors.lastname: Sastre
authors.forename: Cristina
authors.initials: C
authors.lastname: Gámez
authors.forename: Mar
authors.initials: M
authors.lastname: Fernández-Nieto
authors.forename: Joaquín
authors.initials: J
authors.lastname: Sastre
authors.forename: Carlos
authors.initials: C
authors.lastname: Lahoz
authors.forename: Santiago
authors.initials: S
authors.lastname: Quirce
authors.forename: Victoria
authors.initials: V
authors.lastname: Del Pozo
mesh_terms: D000328:Adult; D001249:Asthma / Q000097:blood* / Q000235:genetics / Q000276:immunology / Q000473:pathology; D001991:Bronchitis / Q000097:blood* / Q000235:genetics / Q000276:immunology / Q000473:pathology; D001999:Bronchoscopy; D016022:Case-Control Studies; D002469:Cell Separation; D002478:Cells, Cultured; D015232:Dinoprostone / Q000032:analysis / Q000096:biosynthesis; D004802:Eosinophilia / Q000097:blood* / Q000235:genetics / Q000276:immunology / Q000473:pathology; D004804:Eosinophils / Q000276:immunology / Q000378:metabolism*; D005260:Female; D015870:Gene Expression; D006801:Humans; D008297:Male; D018613:Microscopy, Confocal; D008875:Middle Aged; D015398:Signal Transduction / Q000235:genetics / Q000276:immunology*; D000071223:Suppressor of Cytokine Signaling 3 Protein; D050826:Suppressor of Cytokine Signaling Proteins / Q000235:genetics / Q000378:metabolism*; D018417:Th1 Cells / Q000276:immunology / Q000378:metabolism; D058408:Th1-Th2 Balance; D018418:Th2 Cells / Q000276:immunology / Q000378:metabolism
chemical_list: C106644:SOCS3 protein, human; D000071223:Suppressor of Cytokine Signaling 3 Protein; D050826:Suppressor of Cytokine Signaling Proteins; D015232:Dinoprostone