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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
10
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pubmed:dateCreated |
2009-10-7
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pubmed:abstractText |
We previously demonstrated that IL-7 is essential for the persistence of T-cell-mediated colitis, by showing that adoptive transfer of CD4(+)CD45RB(high) T cells into IL-7(-/-) x RAG-1(-/-) mice did not induce colitis; and that intestinal IL-7 is not essential for this colitis model, by showing that IL-7(-/-) x RAG-1(-/-) mice parabiosed with colitic CD4(+)CD45RB(high) T-cell-transferred RAG-1(-/-) mice developed colitis. Here, we investigated the role of IL-7 in the maintenance of colitogenic CD4(+) T cells by surgically separating these parabionts. Surprisingly, the separated IL-7(-/-) x RAG-1(-/-) mice were consistently diseased after separation, although no IL-7 mRNA was detected in the tissues of separated IL-7(-/-) x RAG-1(-/-) partners. CD4(+) T cells isolated from the separated RAG-1(-/-) or IL-7(-/-) x RAG-1(-/-) mice were then transferred into new RAG-1(-/-) or IL-7(-/-) x RAG-1(-/-) mice. Regardless of the source of donor cells, RAG-1(-/-) recipients developed colitis, whereas IL-7(-/-) x RAG-1(-/-) recipients did not. Collectively, these results demonstrate that IL-7 is essential for lymphopenia-driven turnover of colitogenic CD4(+) T cells rather than the maintenance of those cells in established colitic mice. They also provide a basis for the timing of IL-7/IL-7R blockade for the treatment of inflammatory bowel diseases.
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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 |
Oct
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pubmed:issn |
1521-4141
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pubmed:author |
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pubmed:issnType |
Electronic
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pubmed:volume |
39
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
2737-47
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pubmed:meshHeading |
pubmed-meshheading:19637223-Adoptive Transfer,
pubmed-meshheading:19637223-Animal Structures,
pubmed-meshheading:19637223-Animals,
pubmed-meshheading:19637223-Apoptosis,
pubmed-meshheading:19637223-CD4-Positive T-Lymphocytes,
pubmed-meshheading:19637223-Cell Count,
pubmed-meshheading:19637223-Chronic Disease,
pubmed-meshheading:19637223-Colitis,
pubmed-meshheading:19637223-Colon,
pubmed-meshheading:19637223-DNA-Binding Proteins,
pubmed-meshheading:19637223-Female,
pubmed-meshheading:19637223-Gene Expression,
pubmed-meshheading:19637223-Homeodomain Proteins,
pubmed-meshheading:19637223-Interferon-gamma,
pubmed-meshheading:19637223-Interleukin-15,
pubmed-meshheading:19637223-Interleukin-7,
pubmed-meshheading:19637223-Lymphocyte Subsets,
pubmed-meshheading:19637223-Lymphopenia,
pubmed-meshheading:19637223-Male,
pubmed-meshheading:19637223-Mice,
pubmed-meshheading:19637223-Mice, Inbred C57BL,
pubmed-meshheading:19637223-Mice, Knockout,
pubmed-meshheading:19637223-Mucous Membrane,
pubmed-meshheading:19637223-Parabiosis,
pubmed-meshheading:19637223-Spleen,
pubmed-meshheading:19637223-Tumor Necrosis Factor-alpha
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pubmed:year |
2009
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pubmed:articleTitle |
IL-7 is essential for lymphopenia-driven turnover of colitogenic CD4(+) memory T cells in chronic colitis.
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pubmed:affiliation |
Department of Gastroenterology and Hepatology, Graduate School, Tokyo Medical and Dental University, Tokyo, Japan.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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