Gap junctions between regulatory T cells and dendritic cells prevent sensitization of CD8+ T cells
Background - Regulatory T (Treg) cells suppress the sensitization phase of experimental contact hypersensitivity (CHS) reactions when injected before hapten application. - Objective - Our aim was to analyze the mechanisms by which Treg cells suppress the sensitization phase of CHS reactions. - Metho...
Gespeichert in:
| Hauptverfasser: | , , , , |
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| Dokumenttyp: | Article (Journal) |
| Sprache: | Englisch |
| Veröffentlicht: |
1 January 2010
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| In: |
The journal of allergy and clinical immunology
Year: 2010, Jahrgang: 125, Heft: 1, Pages: 237-246, e1-e7 |
| ISSN: | 1097-6825 |
| DOI: | 10.1016/j.jaci.2009.10.025 |
| Online-Zugang: | Verlag, lizenzpflichtig, Volltext: https://doi.org/10.1016/j.jaci.2009.10.025 Verlag, lizenzpflichtig, Volltext: https://www.sciencedirect.com/science/article/pii/S0091674909015541 
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| Verfasserangaben: | Sabine Ring, PhD, Svetlana Karakhanova, PhD, Theron Johnson, PhD, Alexander H. Enk, MD, and Karsten Mahnke, PhD |
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| 520 | |a Background - Regulatory T (Treg) cells suppress the sensitization phase of experimental contact hypersensitivity (CHS) reactions when injected before hapten application. - Objective - Our aim was to analyze the mechanisms by which Treg cells suppress the sensitization phase of CHS reactions. - Methods - Treg cells were labeled with different fluorescent dyes and injected into naive mice directly before sensitization with the hapten 2,4,6-trinitro-1-chlorobenzene. Two days after sensitization, the lymphoid organs were analyzed for the presence of Treg cells and engagement of gap junctions with other cells. Dendritic cells (DCs) and effector CD8+T cells were isolated from the draining lymph nodes (LNs) of the differently treated groups, analyzed by using FACS for activation markers, and assessed for the T-cell stimulatory capacity of the DCs and the priming of effector T cells. - Results - Only the LN-homing Treg cells suppressed the sensitization phase in CHS reactions by means of establishing gap junctions with DCs in the dLNs. This gap junctional intercellular communication led to downregulation of T-cell costimulatory molecules on the surface of the DCs, abrogating the priming, activation, and proliferation of hapten-specific CD8+T cells. Consequently, the ear-swelling response induced by challenge with the respective hapten was prevented. - Conclusion - Treg cells not only modulate ongoing CD4+T cell-mediated immune reactions at tissue sites but also abrogate the de novo induction of CD8+T cell-driven immune reactions by interfering with T-cell stimulatory activity of DCs through gap junctional intercellular communication. | ||
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