PMID- 21937446
OWN - NLM
STAT- MEDLINE
DCOM- 20111227
LR  - 20211020
IS  - 1083-351X (Electronic)
IS  - 0021-9258 (Print)
IS  - 0021-9258 (Linking)
VI  - 286
IP  - 45
DP  - 2011 Nov 11
TI  - Intranodal interaction with dendritic cells dynamically regulates surface 
      expression of the co-stimulatory receptor CD226 protein on murine T cells.
PG  - 39153-63
LID - 10.1074/jbc.M111.264697 [doi]
AB  - Dendritic cells (DCs) are the most potent antigen-presenting cells of the immune 
      system. Depending on their maturation status, they prime T cells to induce 
      adaptive immunity or tolerance. DCs express CD155, an immunoglobulin-like 
      receptor binding CD226 present on T and natural killer (NK) cells. CD226 
      represents an important co-stimulator during T cell priming but also serves as an 
      activating receptor on cytotoxic T and NK cells. Here, we report that cells of 
      the T and NK cell lineage of CD155(-/-) mice express markedly elevated protein 
      levels of CD226 compared with wild type (WT). On heterozygous CD155(+/-) T cells, 
      CD226 up-regulation is half-maximal, implying an inverse gene-dosis effect. 
      Moreover, CD226 up-regulation is independent of antigen-driven activation because 
      it occurs already in thymocytes and naive peripheral T cells. In vivo, 
      neutralizing anti-CD155 antibody elicits up-regulation of CD226 on T cells 
      demonstrating, that the observed modulation can be triggered by interrupting 
      CD155-CD226 contacts. Adoptive transfers of WT or CD155(-/-) T cells into 
      CD155(-/-) or WT recipients, respectively, revealed that CD226 modulation is 
      accomplished in trans. Analysis of bone marrow chimeras showed that regulators in 
      trans are of hematopoietic origin. We demonstrate that DCs are capable of 
      manipulating CD226 levels on T cells in vivo but not in vitro, suggesting that 
      the process of T cells actively scanning antigen-presenting DCs inside secondary 
      lymphoid organs is required for CD226 modulation. Hence, a CD226 level divergent 
      from WT may be exploited as a sensor to detect abnormal DC/T-cell cross-talk as 
      illustrated for T cells in mice lacking CCR7.
FAU - Seth, Sebastian
AU  - Seth S
AD  - Institute of Immunology, Hannover Medical School, D-30625 Hannover, Germany.
FAU - Qiu, Quan
AU  - Qiu Q
FAU - Danisch, Simon
AU  - Danisch S
FAU - Maier, Michael K
AU  - Maier MK
FAU - Braun, Asolina
AU  - Braun A
FAU - Ravens, Inga
AU  - Ravens I
FAU - Czeloth, Niklas
AU  - Czeloth N
FAU - Hyde, Rebecca
AU  - Hyde R
FAU - Dittrich-Breiholz, Oliver
AU  - Dittrich-Breiholz O
FAU - Forster, Reinhold
AU  - Forster R
FAU - Bernhardt, Gunter
AU  - Bernhardt G
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20110921
PL  - United States
TA  - J Biol Chem
JT  - The Journal of biological chemistry
JID - 2985121R
RN  - 0 (Antibodies, Neutralizing)
RN  - 0 (Antigens, Differentiation, T-Lymphocyte)
RN  - 0 (CD226 antigen)
RN  - 0 (Ccr7 protein, mouse)
RN  - 0 (Receptors, CCR7)
RN  - 0 (Receptors, Virus)
RN  - 0 (poliovirus receptor)
SB  - IM
MH  - Adoptive Transfer
MH  - Animals
MH  - Antibodies, Neutralizing/pharmacology
MH  - Antigens, Differentiation, T-Lymphocyte/biosynthesis/genetics/*immunology
MH  - Cell Communication/drug effects/genetics/*immunology
MH  - Dendritic Cells/cytology/*immunology/metabolism
MH  - Lymph Nodes/cytology/*immunology/metabolism
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - Mice, Knockout
MH  - Receptors, CCR7/genetics/immunology/metabolism
MH  - Receptors, Virus/antagonists & inhibitors/genetics/immunology/metabolism
MH  - T-Lymphocytes/cytology/*immunology/metabolism
MH  - Up-Regulation/drug effects/genetics/*immunology
PMC - PMC3234740
EDAT- 2011/09/23 06:00
MHDA- 2011/12/28 06:00
PMCR- 2012/11/11
CRDT- 2011/09/23 06:00
PHST- 2011/09/23 06:00 [entrez]
PHST- 2011/09/23 06:00 [pubmed]
PHST- 2011/12/28 06:00 [medline]
PHST- 2012/11/11 00:00 [pmc-release]
AID - S0021-9258(20)50574-7 [pii]
AID - M111.264697 [pii]
AID - 10.1074/jbc.M111.264697 [doi]
PST - ppublish
SO  - J Biol Chem. 2011 Nov 11;286(45):39153-63. doi: 10.1074/jbc.M111.264697. Epub 
      2011 Sep 21.