title: Chlamydia infection induces ICOS ligand-expressing and IL-10-producing dendritic cells that can inhibit airway inflammation and mucus overproduction elicited by allergen challenge in BALB/c mice.
abstract: Our previous study has shown that the adoptive transfer of dendritic cells (DCs) freshly isolated from Chlamydia-infected mice (iIDCs), unlike those from control naive mice (iNDCs), can inhibit systemic and cutaneous eosinophilia induced by OVA exposure. In the present study, we examined the mechanism by which iIDC inhibits allergen-specific Th2 cell differentiation in vitro and in vivo. The study revealed that iIDCs exhibited higher surface expression of CD8alpha and the ICOS ligand (ICOS-L), as well as higher IL-10 and IL-12 production than iNDCs. In vitro DC:CD4(+) T cell coculture experiments showed that iIDCs could inhibit allergen-specific Th2 cell differentiation and that the inhibitory effect could be abolished by the blockage of IL-10 or IL-12 activity. More interestingly, the coblockade of IL-10 and the ICOS-L showed synergistic effect in enhancing allergen-driven Th2 cytokine production. Furthermore, adoptive transfer of iIDCs, but not iNDCs, to OVA sensitized mice significantly inhibited airway eosinophilia and mucus overproduction following intranasal challenge with OVA. Overall, the data demonstrate a critical role played by ICOS-L-expressing and IL-10-producing DCs from Chlamydia-infected mice in the infection-mediated inhibition of allergic responses.
authors.affiliation: Immune Regulation of Allergy Research Group, Departments of Medical Microbiology and Immunology, Faculty of Medicine, University of Manitoba, 730 William Avenue, Winnipeg, Manitoba, Canada.
authors.forename: Xiaobing
authors.initials: X
authors.lastname: Han
authors.forename: Shuhe
authors.initials: S
authors.lastname: Wang
authors.forename: Yijun
authors.initials: Y
authors.lastname: Fan
authors.forename: Jie
authors.initials: J
authors.lastname: Yang
authors.forename: Lei
authors.initials: L
authors.lastname: Jiao
authors.forename: Hongyu
authors.initials: H
authors.lastname: Qiu
authors.forename: Xi
authors.initials: X
authors.lastname: Yang
mesh_terms: D000485:Allergens / Q000276:immunology / Q000378:metabolism; D000818:Animals; D015496:CD4-Positive T-Lymphocytes / Q000187:drug effects / Q000276:immunology / Q000378:metabolism; D002454:Cell Differentiation / Q000187:drug effects; D002469:Cell Separation; D002478:Cells, Cultured; D054413:Chemokine CCL11; D019742:Chemokines, CC / Q000378:metabolism; D002689:Chlamydia / Q000502:physiology*; D002690:Chlamydia Infections / Q000276:immunology / Q000378:metabolism* / Q000382:microbiology / Q000473:pathology; D003713:Dendritic Cells / Q000276:immunology / Q000378:metabolism*; D004802:Eosinophilia / Q000276:immunology; D005088:Exocrine Glands / Q000276:immunology / Q000378:metabolism; D005260:Female; D005786:Gene Expression Regulation; D060945:Inducible T-Cell Co-Stimulator Ligand; D016753:Interleukin-10 / Q000096:biosynthesis*; D018664:Interleukin-12 / Q000096:biosynthesis; D051379:Mice; D008807:Mice, Inbred BALB C; D009093:Mucus / Q000276:immunology / Q000378:metabolism*; D010047:Ovalbumin / Q000494:pharmacology; D011014:Pneumonia / Q000276:immunology / Q000378:metabolism* / Q000382:microbiology / Q000473:pathology; D011506:Proteins / Q000378:metabolism*; D019010:Vascular Cell Adhesion Molecule-1 / Q000378:metabolism
chemical_list: D000485:Allergens; C515457:Ccl11 protein, mouse; D054413:Chemokine CCL11; D019742:Chemokines, CC; C400230:Icosl protein, mouse; D060945:Inducible T-Cell Co-Stimulator Ligand; D011506:Proteins; D019010:Vascular Cell Adhesion Molecule-1; D016753:Interleukin-10; D018664:Interleukin-12; D010047:Ovalbumin