γδ T cells support gut Ag‐reactive colitogenic effector T‐cell generation by enhancing Ag presentation by CD11b+ DCs in the mesenteric LN

T cells expressing the γδ TCR are dominant T‐cell subsets in the intestinal immune system. We previously demonstrated that γδ T cells play important roles in augmenting Th17‐type colitogenic immune responses in a T‐cell‐induced colitic inflammation model. However, its underlying mechanism remains po...

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Bibliographic Details
Published in:European journal of immunology 2016-02, Vol.46 (2), p.340-346
Main Authors: Do, Jeongsu, Visperas, Anabelle, Freeman, Michael L., Jang, Eunjung, Kim, Sohee, Malissen, Bernard, Min, Booki
Format: Article
Language:English
Subjects:
Animals
Antigen Presentation
Cells, Cultured
Colitis
Colitis - immunology
DCs
Dendritic Cells - immunology
Disease Models, Animal
Gut Ag
Humans
Immunity, Mucosal
Intestines - immunology
Lymph Nodes - immunology
Mesentery - pathology
Mice
Mice, Inbred C57BL
Mice, Knockout
Receptors, Antigen, T-Cell, gamma-delta - metabolism
T-Lymphocyte Subsets - metabolism
Th17 Cells - immunology
γδ T cells
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Summary:T cells expressing the γδ TCR are dominant T‐cell subsets in the intestinal immune system. We previously demonstrated that γδ T cells play important roles in augmenting Th17‐type colitogenic immune responses in a T‐cell‐induced colitic inflammation model. However, its underlying mechanism remains poorly understood. In this study, an in vitro coculture system using effector T cells enriched in gut Ag‐reactive cells was employed as a readout tool to search for gut Ag presenting APCs. We found that the presence of γδ T cells dramatically enhances gut Ag presentation within the mLN in mice. Gut Ag presentation by CD11b+ DC subsets was particularly controlled by γδ T cells. Interestingly, γδ T‐cell entry to the lymph nodes was essential to improve the Ag presentation. Therefore, our results highlight that γδ T cells play a previously unrecognized role to support colitogenic immunity by regulating gut Ag presentation in the draining LN.
ISSN:0014-2980
1521-4141
DOI:10.1002/eji.201545919