title: Eosinophils from hematopoietic stem cell recipients suppress allogeneic T cell proliferation.
abstract: Eosinophilia has been associated with less severe graft-versus-host disease (GVHD), but the underlying mechanism is unknown. We hypothesized that eosinophils diminish allogeneic T cell activation in patients with chronic GVHD. The capacity of eosinophils derived from healthy subjects and hematopoietic stem cell (HSC) transplant recipients, with or without chronic GVHD, to reduce allogeneic T cell proliferation was evaluated using a mixed leukocyte reaction. Eosinophil-mediated inhibition of proliferation was observed for the eosinophils of both healthy subjects and patients who underwent HSC transplantation. Eosinophils from patients with and without chronic GVHD were equally suppressive. Healthy eosinophils required cell-to-cell contact for their suppressive capacity, which was directed against CD4(+) T cells and CD8(+) T cells. Neither eosinophilic cationic protein, eosinophil-derived neurotoxin, indoleamine 2,3-dioxygenase, or increased numbers of regulatory T cells could account for the suppressive effect of healthy eosinophils. Real-time quantitative PCR analysis revealed significantly increased mRNA levels of the immunoregulatory protein galectin-10 in the eosinophils of both chronic GVHD patients and patients without GVHD, as compared with those from healthy subjects. The upregulation of galectin-10 expression in eosinophils from patients suggests a stimulatory effect of HSC transplantation in itself on eosinophilic galectin-10 expression, regardless of chronic GVHD status. To conclude, eosinophils from HSC transplant recipients and healthy subjects have a T cell suppressive capacity.
authors.affiliation: Department of Infectious Diseases, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden. Electronic address: jennie.andersson@microbio.gu.se.
authors.forename: Jennie
authors.initials: J
authors.lastname: Andersson
authors.affiliation: Department of Hematology and Coagulation, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
authors.forename: Julia
authors.initials: J
authors.lastname: Cromvik
authors.affiliation: Department of Infectious Diseases, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
authors.forename: Madeleine
authors.initials: M
authors.lastname: Ingelsten
authors.affiliation: Department of Infectious Diseases, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
authors.forename: Christine
authors.initials: C
authors.lastname: Lingblom
authors.affiliation: Department of Infectious Diseases, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
authors.forename: Kerstin
authors.initials: K
authors.lastname: Andersson
authors.affiliation: Department of Hematology and Coagulation, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
authors.forename: Jan-Erik
authors.initials: JE
authors.lastname: Johansson
authors.affiliation: Department of Infectious Diseases, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
authors.forename: Christine
authors.initials: C
authors.lastname: Wennerås
mesh_terms: D000328:Adult; D000368:Aged; D064591:Allografts; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology* / Q000473:pathology; D018414:CD8-Positive T-Lymphocytes / Q000276:immunology* / Q000473:pathology; D002908:Chronic Disease; D004804:Eosinophils / Q000276:immunology* / Q000473:pathology; D005260:Female; D037161:Galectins / Q000276:immunology*; D006086:Graft vs Host Disease / Q000209:etiology / Q000276:immunology* / Q000473:pathology; D018380:Hematopoietic Stem Cell Transplantation; D006801:Humans; D008297:Male; D008875:Middle Aged; D015854:Up-Regulation / Q000276:immunology
chemical_list: D037161:Galectins; C523496:galectin 10, human
keywords: Eosinophil; Galectin-10; Graft-versus-host disease; Suppression; T cell inflammation