title: Adoptive transfer of dendritic cells isolated from helminth-infected mice enhanced T regulatory cell responses in airway allergic inflammation.
abstract: Our and others' previous studies have shown that Schistosoma japonicum (SJ) infection can inhibit allergic reactions. Moreover, we found that adoptive transfer of dendritic cells (DCs) from inhibited mice showed a similar inhibitory effect on allergy, suggesting a critical role of DCs in SJ-infected mediated inhibition of allergy. In this study, we further examined the mechanism by which DCs contribute to inhibition of allergy. Our results showed that DCs from SJ-infected mice (SJDCs) produced significantly higher levels of IL-10 compared to those from naive control mice (NDCs). Adoptive transfer of SJDCs, unlike NDCs, significantly increased CD4+CD25+Foxp3+ T cells and CD4+CD25+IL-10+ T cells regulatory T-cell responses in vivo. This was correlated with significantly reduced production of IL-4 and IL-5 by CD4+ T cells, eotaxin in lung tissues and reduced airway allergic inflammation in the SJDC recipients following allergen sensitization and challenge. These data suggest that helminth infection may induce tolerogenic DCs that can inhibit the development of airway allergic inflammation through enhancing T regulatory cell responses.
authors.affiliation: Laboratory of Cellular and Molecular Immunology, Department of Parasitology, Faculty of Basic Medicine Sciences, Tianjin Medical University, Tianjin, China.
authors.forename: J-Y
authors.initials: JY
authors.lastname: Liu
authors.forename: L-Y
authors.initials: LY
authors.lastname: Li
authors.forename: X-Z
authors.initials: XZ
authors.lastname: Yang
authors.forename: J
authors.initials: J
authors.lastname: Li
authors.forename: G
authors.initials: G
authors.lastname: Zhong
authors.forename: J
authors.initials: J
authors.lastname: Wang
authors.forename: L-J
authors.initials: LJ
authors.lastname: Li
authors.forename: B
authors.initials: B
authors.lastname: Ji
authors.forename: Z-Q
authors.initials: ZQ
authors.lastname: Wu
authors.forename: H
authors.initials: H
authors.lastname: Liu
authors.forename: X
authors.initials: X
authors.lastname: Yang
authors.forename: P-M
authors.initials: PM
authors.lastname: Liu
mesh_terms: D019264:Adoptive Transfer / Q000379:methods*; D000818:Animals; D015704:CD4 Antigens / Q000032:analysis; D054413:Chemokine CCL11 / Q000378:metabolism; D003713:Dendritic Cells / Q000276:immunology*; D005260:Female; D051858:Forkhead Transcription Factors / Q000032:analysis; D007249:Inflammation / Q000276:immunology / Q000473:pathology; D016753:Interleukin-10 / Q000378:metabolism; D053645:Interleukin-2 Receptor alpha Subunit / Q000032:analysis; D015847:Interleukin-4 / Q000378:metabolism; D015848:Interleukin-5 / Q000378:metabolism; D008168:Lung / Q000276:immunology / Q000473:pathology; D051379:Mice; D008807:Mice, Inbred BALB C; D012130:Respiratory Hypersensitivity / Q000628:therapy*; D012554:Schistosomiasis japonica / Q000276:immunology*; D016176:T-Lymphocyte Subsets / Q000276:immunology; D050378:T-Lymphocytes, Regulatory / Q000737:chemistry / Q000276:immunology*
chemical_list: D015704:CD4 Antigens; D054413:Chemokine CCL11; D051858:Forkhead Transcription Factors; C498833:Foxp3 protein, mouse; C508018:Il2ra protein, mouse; D053645:Interleukin-2 Receptor alpha Subunit; D015848:Interleukin-5; D016753:Interleukin-10; D015847:Interleukin-4