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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
1
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pubmed:dateCreated |
2003-1-9
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pubmed:abstractText |
Adoptive transfer of CD4+ T cells into scid mice leads to a chronic colitis in the recipients. The transferred CD4+ T cells accumulate in the intestinal lamina propria (LP), express an activated Th1 phenotype and proliferate vigorously when exposed ex vivo to enteric bacterial antigens. As LP CD4+ T cells from normal BALB/c mice do not respond to enteric bacterial antigens, we have investigated whether colonic LP-derived CD4+ T cells from normal mice suppress the antibacterial response of CD4+ T cells from scid mice with colitis. LP-derived CD4+ T cells cocultured with bone marrow-derived dendritic cells effectively suppress the antibacterial proliferative response of CD4+ T cells from scid mice with colitis. The majority of these LP T-reg cells display a nonactivated phenotype and suppression is independent of antigen exposure, is partly mediated by soluble factor(s) different from IL-10 and TGF-beta, and is not prevented by the addition of high doses of IL-2 to the assay culture. Functionally and phenotypically the T-reg cells of the present study differ from previously described subsets of T-reg cells. The presence of T cells with a regulatory potential in the normal colonic mucosa suggests a role for these cells in the maintenance of local immune homeostasis of the gut.
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/12519383-10092833,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12519383-10228007,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12519383-10329996,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12519383-10500290,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12519383-10510089,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12519383-10605010,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12519383-10632969,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12519383-10750645,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12519383-10837065,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12519383-10872893,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12519383-10899916,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12519383-10899917,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12519383-11067871,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12519383-11102772,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12519383-11169434,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12519383-11390442,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12519383-12093005,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12519383-2960770,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12519383-7687523,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12519383-7903159,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12519383-8100269,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12519383-8536356,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12519383-8647181,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12519383-8676088,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12519383-9057354,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12519383-9238837,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12519383-9338786,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12519383-9500788,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12519383-9620592,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12519383-9670041,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12519383-9815262,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12519383-9862840,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12519383-9885918
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Jan
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pubmed:issn |
0009-9104
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
131
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
34-40
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pubmed:dateRevised |
2009-11-18
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pubmed:meshHeading |
pubmed-meshheading:12519383-Adoptive Transfer,
pubmed-meshheading:12519383-Animals,
pubmed-meshheading:12519383-Antigens, Bacterial,
pubmed-meshheading:12519383-CD4-Positive T-Lymphocytes,
pubmed-meshheading:12519383-Cell Division,
pubmed-meshheading:12519383-Colon,
pubmed-meshheading:12519383-Enterobacteriaceae,
pubmed-meshheading:12519383-Enterobacteriaceae Infections,
pubmed-meshheading:12519383-Inflammatory Bowel Diseases,
pubmed-meshheading:12519383-Intestinal Mucosa,
pubmed-meshheading:12519383-Mice,
pubmed-meshheading:12519383-Mice, SCID,
pubmed-meshheading:12519383-Th1 Cells
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pubmed:year |
2003
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pubmed:articleTitle |
CD4+ T regulatory cells from the colonic lamina propria of normal mice inhibit proliferation of enterobacteria-reactive, disease-inducing Th1-cells from scid mice with colitis.
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pubmed:affiliation |
Department of Medical Anatomy A, Panum Institute, University of Copenhagen, Copenhagen, Denmark.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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