PMID- 20109751
OWN - NLM
STAT- MEDLINE
DCOM- 20100225
LR  - 20100129
IS  - 1097-6825 (Electronic)
IS  - 0091-6749 (Linking)
VI  - 125
IP  - 1
DP  - 2010 Jan
TI  - Gap junctions between regulatory T cells and dendritic cells prevent 
      sensitization of CD8(+) T cells.
PG  - 237-46.e1-7
LID - 10.1016/j.jaci.2009.10.025 [doi]
AB  - 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.
CI  - Copyright 2010 American Academy of Allergy, Asthma & Immunology. Published by 
      Mosby, Inc. All rights reserved.
FAU - Ring, Sabine
AU  - Ring S
AD  - Department of Dermatology, University Hospital Heidelberg, Vossstrasse 11, 69115 
      Heidelberg, Germany. Sabine.Ring@med.uni-heidelberg.de
FAU - Karakhanova, Svetlana
AU  - Karakhanova S
FAU - Johnson, Theron
AU  - Johnson T
FAU - Enk, Alexander H
AU  - Enk AH
FAU - Mahnke, Karsten
AU  - Mahnke K
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Allergy Clin Immunol
JT  - The Journal of allergy and clinical immunology
JID - 1275002
RN  - 0 (Haptens)
SB  - IM
MH  - Animals
MH  - CD8-Positive T-Lymphocytes/*immunology
MH  - Dendritic Cells/cytology/*immunology
MH  - Dermatitis, Contact/*immunology
MH  - Flow Cytometry
MH  - Gap Junctions/*physiology
MH  - Haptens/immunology
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - Mice, Inbred C57BL
MH  - T-Lymphocytes, Regulatory/cytology/*immunology
EDAT- 2010/01/30 06:00
MHDA- 2010/02/26 06:00
CRDT- 2010/01/30 06:00
PHST- 2009/03/19 00:00 [received]
PHST- 2009/09/28 00:00 [revised]
PHST- 2009/10/06 00:00 [accepted]
PHST- 2010/01/30 06:00 [entrez]
PHST- 2010/01/30 06:00 [pubmed]
PHST- 2010/02/26 06:00 [medline]
AID - S0091-6749(09)01554-1 [pii]
AID - 10.1016/j.jaci.2009.10.025 [doi]
PST - ppublish
SO  - J Allergy Clin Immunol. 2010 Jan;125(1):237-46.e1-7. doi: 
      10.1016/j.jaci.2009.10.025.