title: Concurrent exposure to a dectin-1 agonist suppresses the Th2 response to epicutaneously introduced antigen in mice.
abstract: BACKGROUND
  Epicutaneous sensitization with protein allergen that induces predominant Th2 responses is an important sensitization route in atopic dermatitis. Fungal components have been shown to modulate Th cell differentiation. However, the effects of fungal components on epicutaneous sensitization are unclear.
  
  
  RESULTS
  In this study, we showed that co-administration of curdlan, a dectin-1 agonist, during epicutaneous ovalbumin sensitization of BALB/c mice decreased the IL-5 and IL-13 levels in supernatants of lymph node cell ovalbumin reactivation cultures. Mechanistically, curdlan co-administration decreased IL-4 and IL-1β expressions in draining lymph nodes. Curdlan co-administration also lower the migration of langerin+ CD103- epidermal Langerhans cells into draining lymph nodes at 96 hours post-sensitization which might be attributed to decreased expressions of IL-18 and IL-1β in patched skin. Moreover, adoptive transfer of CFSE-labeled transgenic CD4 T cells confirmed that curdlan co-administration decreased the proliferation and IL-4-production of ovalbumin -specific T cells primed by epidermal Langerhans cells.
  
  
  CONCLUSIONS
  These results indicated that concurrent exposure to a dectin-1 agonist suppresses the epicutaneously induced Th2 response by modulating the cytokine expression profiles in draining LNs and the migration of epidermal Langerhans cells. These results highlight the effects of fungal components on epicutaneous allergen sensitization in atopic diseases.
authors.affiliation: Department of Dermatology, Chang Gung Memorial Hospital, Chang Gung University College of Medicine, Taoyuan, Taiwan.
authors.forename: Jing-Yi
authors.initials: JY
authors.lastname: Lin
authors.forename: Jau-Shiuh
authors.initials: JS
authors.lastname: Chen
authors.forename: Pei-Chun
authors.initials: PC
authors.lastname: Chen
authors.forename: Ming-Hui
authors.initials: MH
authors.lastname: Chung
authors.forename: Ching-Yi
authors.initials: CY
authors.lastname: Liu
authors.forename: Shi-Chuen
authors.initials: SC
authors.lastname: Miaw
authors.forename: Li-Fang
authors.initials: LF
authors.lastname: Wang
mesh_terms: D000279:Administration, Cutaneous; D000485:Allergens / Q000276:immunology / Q000378:metabolism; D000818:Animals; D000954:Antigens, Surface / Q000378:metabolism; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology / Q000378:metabolism; D002465:Cell Movement / Q000276:immunology; D003876:Dermatitis, Atopic / Q000378:metabolism / Q000473:pathology; D018793:Interleukin-13 / Q000276:immunology / Q000378:metabolism; D015848:Interleukin-5 / Q000276:immunology / Q000378:metabolism; D037181:Lectins, C-Type / Q000819:agonists / Q000276:immunology* / Q000378:metabolism; D008198:Lymph Nodes / Q000276:immunology* / Q000378:metabolism; D037241:Mannose-Binding Lectins / Q000378:metabolism; D051379:Mice; D008807:Mice, Inbred BALB C; D010047:Ovalbumin / Q000378:metabolism*; D018418:Th2 Cells / Q000166:cytology / Q000276:immunology* / Q000378:metabolism; D047071:beta-Glucans / Q000008:administration & dosage*; D000099181:Dectin-1
chemical_list: D000485:Allergens; D000954:Antigens, Surface; D018793:Interleukin-13; D015848:Interleukin-5; D037181:Lectins, C-Type; D037241:Mannose-Binding Lectins; D010047:Ovalbumin; D047071:beta-Glucans; D000099181:Dectin-1; C498497:Cd207 protein, mouse; C038459:curdlan