Impaired function of dendritic cells in alymphoplasia (aly/aly) mice for expansion of CD25+CD4+regulatory T cells
Autor: | Mutsuhiko Minami, Chizuru Tamura, Masaki Kasahara, Chie Hotta, Fumitaka Sato, Masatoshi Nakazawa, Masahiro Yoshinari |
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Rok vydání: | 2006 |
Předmět: |
Ovalbumin
animal diseases Genes MHC Class II Immunology Antigen presentation Mice Transgenic chemical and pharmacologic phenomena T-Lymphocytes Regulatory Mice Animals Immunology and Allergy IL-2 receptor Antigen-presenting cell Lymphatic Diseases Cells Cultured CD86 Antigen Presentation Mice Inbred BALB C MHC class II biology Interleukin-2 Receptor alpha Subunit Cell Differentiation hemic and immune systems Dendritic Cells T lymphocyte Dendritic cell respiratory system Molecular biology respiratory tract diseases Mice Inbred C57BL CD4 Antigens B7-1 Antigen biology.protein B7-2 Antigen Spleen CD80 |
Zdroj: | Autoimmunity. 39:445-453 |
ISSN: | 1607-842X 0891-6934 |
Popis: | Alymphoplasia (aly/aly) mice are from a naturally occurring strain with a mutation in nuclear factor-kappa B inducing kinase (NIK). The NIK mutation causes disruption of the architecture of the thymus and spleen and aly/aly mice show decreased numbers of CD25+CD4+T cells in the spleen. For the expansion of CD25+CD4+T cells, interactions between dendritic cells (DCs) and CD25+CD4+ regulatory T cells are necessary. We investigated the ability of DCs to induce expansion of CD25+CD4+T cells. We found that DCs are reduced in the spleen of aly/aly mice, and showed low expressions of CD80, CD86 and MHC class II molecules on the surface. DCs from aly/aly mice showed decreased ability to present ovalbumin (OVA) to T cells from OVA specific TCR transgenic mice, and a decreased ability for alloantigen presentation. Further, DCs showed a decreased ability to induce expansion of CD25+CD4+T cells in vitro. Our results suggested that the impairment of DCs in aly/aly mice is responsible, at least in part, for the decreased numbers of CD25+CD4+T cells in the periphery of aly/aly mice. |
Databáze: | OpenAIRE |
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