0000000000498437

AUTHOR

Junichi Hirahashi

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Inducible Co-Stimulator Null MRL-Fas lpr Mice

2005

MRL/MpJ-Tnfrsf6lpr (MRL-Faslpr) mice develop a spontaneous T cell-dependent autoimmune disease that shares features with human lupus, including fatal nephritis, systemic pathology, and autoantibodies (autoAb). The inducible co-stimulator (ICOS) is upregulated on activated T cells and modulates T cell-mediated responses. To investigate whether ICOS has an essential role in regulating autoimmune lupus nephritis and the systemic illness in MRL-Faslpr mice, ICOS null (-/-) MRL Faslpr and ICOS intact (+/+) MRL-Faslpr strains (wild-type [WT]) were generated and compared. It was determined that in ICOS-/- MRL-Faslpr as compared with the WT strain, (1) there is a significant reduction in circulatin…

Antigens Differentiation T-LymphocyteMice Inbred MRL lprT-LymphocytesT cellLupus nephritismedicine.disease_causeBlood Urea NitrogenAutoimmunityInducible T-Cell Co-Stimulator ProteinInterferon-gammaMiceImmune systemimmune system diseasesmedicineAnimalsskin and connective tissue diseasesAutoantibodiesMice Inbred C3HSystemic lupus erythematosusTumor Necrosis Factor-alphabusiness.industryAutoantibodyGeneral Medicinemedicine.diseaseLupus NephritisIsotypeInterleukin-10Mice Inbred C57BLProteinuriamedicine.anatomical_structureNephrologyImmunoglobulin GImmunologyInterleukin-4businessNephritisJournal of the American Society of Nephrology
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