Document
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Journal of Immunology
publication venue for: CCL22-producing CD8α- myeloid dendritic cells mediate regulatory T cell recruitment in response to G-CSF treatment
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type: Periodical
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RDF description of CCL22-producing CD8α- myeloid dendritic cells mediate regulatory T cell recruitment in response to G-CSF treatment - http://orbis.uaslp.mx/vivo/individual/scopus3463
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date: 2026-08-24T21:45:42
publisher: vivo
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Article
type: Class

CCL22-producing CD8α- myeloid dendritic cells mediate regulatory T cell recruitment in response to G-CSF treatment
abstract: G-CSF prevents type 1 diabetes in the NOD mouse by promoting the local recruitment of T regulatory cells (Tregs). This is an indirect effect because adoptive transfer of G-CSF-induced tolerogenic dendritic cells (DCs) promotes Treg accumulation. However, the identity of the particular DC subset and the molecule(s) mediating this effect remain unknown. We demonstrate in this study that the adoptive transfer of CD11chighCD8α- DCs isolated from pegylated G-CSF (pegG-CSF) recipients, but not that of other DC subtypes, enhanced the pancreatic recruitment of CD4%2bCD25 %2bFoxp3%2b Tregs, which generated increased amounts of TGF-β. Likewise, only CD11chighCD8α- DCs from pegG-CSF recipients secreted the chemokine CCL22 at levels that effectively attracted Tregs. PegG-CSF was more efficient at enhancing the synthesis of CCL22 by CD11chighCD8α- DCs from the pancreatic lymph nodes compared with those from the spleen. Accordingly, CD11c highCD8α- DCs from the pancreatic lymph nodes of pegG-CSF recipients were more efficient than their splenic counterparts in the recruitment of Tregs upon adoptive transfer. Predictably, CD11c highCD8α- DCs failed to recruit these Tregs both in vivo and in vitro following intracellular neutralization of CCL22. These data assign a key role to CD8α- DCs and CCL22 in Treg recruitment in the protection of NOD mice against type 1 diabetes following the treatment with G-CSF. Copyright © 2013 by The American Association of Immunologists, Inc.
e iscopus: 2-s2.0-84883354718
date time value: article date 3464
type: Continuant
doi: 10.4049/jimmunol.1202307
related by: authorship_19979
freetext keyword: CD4 antigen; CD8alpha antigen; glycoprotein p 15095; interleukin 2 receptor alpha; macrophage derived chemokine; pegylated granulocyte colony stimulating factor; recombinant cytokine; transcription factor FOXP3; transforming growth factor beta; unclassified drug; adoptive transfer; animal cell; animal experiment; animal model; article; cell isolation; cell stimulation; controlled study; cytokine production; female; in vitro study; in vivo study; insulin dependent diabetes mellitus; lymph node; mouse; myeloid dendritic cell; nonhuman; nonobese diabetic mouse; priority journal; protection; protein function; regulatory T lymphocyte; spleen; tissue specificity; Adoptive Transfer; Animals; Antigens, CD8; Chemokine CCL2; Chemotaxis, Leukocyte; Dendritic Cells; Diabetes Mellitus, Type 1; Enzyme-Linked Immunosorbent Assay; Flow Cytometry; Granulocyte Colony-Stimulating Factor; Mice; Mice, Inbred NOD; Myeloid Cells; Reverse Transcriptase Polymerase Chain Reaction; T-Lymphocytes, Regulatory
type: Thing
most specific type: Document
crisid: 3464
type: Document
pmid: 23878314
accesstype: All Open Access, Bronze
abstract: G-CSF prevents type 1 diabetes in the NOD mouse by promoting the local recruitment of T regulatory cells (Tregs). This is an indirect effect because adoptive transfer of G-CSF-induced tolerogenic dendritic cells (DCs) promotes Treg accumulation. However, the identity of the particular DC subset and the molecule(s) mediating this effect remain unknown. We demonstrate in this study that the adoptive transfer of CD11chighCD8α- DCs isolated from pegylated G-CSF (pegG-CSF) recipients, but not that of other DC subtypes, enhanced the pancreatic recruitment of CD4 CD25 Foxp3 Tregs, which generated increased amounts of TGF-β. Likewise, only CD11chighCD8α- DCs from pegG-CSF recipients secreted the chemokine CCL22 at levels that effectively attracted Tregs. PegG-CSF was more efficient at enhancing the synthesis of CCL22 by CD11chighCD8α- DCs from the pancreatic lymph nodes compared with those from the spleen. Accordingly, CD11c highCD8α- DCs from the pancreatic lymph nodes of pegG-CSF recipients were more efficient than their splenic counterparts in the recruitment of Tregs upon adoptive transfer. Predictably, CD11c highCD8α- DCs failed to recruit these Tregs both in vivo and in vitro following intracellular neutralization of CCL22. These data assign a key role to CD8α- DCs and CCL22 in Treg recruitment in the protection of NOD mice against type 1 diabetes following the treatment with G-CSF. Copyright © 2013 by The American Association of Immunologists, Inc.
issue: 5
page start: 2266
type: Entity
related by: authorship_19978
page end: 2272
related by: authorship_19985
related by: authorship_19981
type: Information Content Entity
related by: authorship_19982
type: Article
type: Generically Dependent Continuant
has publication venue: Journal of Immunology
most specific type: Article
estado: published
origen: scopus
related by: authorship_19983
chemicalscas: Antigens, CD8; CD8 antigen, alpha chain; Ccl2 protein, mouse; Chemokine CCL2; Granulocyte Colony-Stimulating Factor, 143011-72-7
volume: 191
related by: authorship_19984
related by: authorship_19980

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