Fibrosis of organs is observed in systemic autoimmune disease. Using a scleroderma\nmouse, we show that transplantation of MHC compatible, minor antigen mismatched bone marrow\nstromal/stem cells (BMSCs) play a role in the pathogenesis of fibrosis. Removal of donor BMSCs\nrescued mice from disease. Freshly isolated PDGFRa\n+ Sca-1+ BMSCs expressed MHC class II\nfollowing transplantation and activated host T cells. A decrease in FOXP3+ CD25+ Treg population\nwas observed. T cells proliferated and secreted IL-6 when stimulated with mismatched BMSCs in\nvitro. Donor T cells were not involved in fibrosis because transplanting T cell-deficient RAG2 knock\nout mice bone marrow still caused disease. Once initially triggered by mismatched BMSCs, the\nautoimmune phenotype was not donor BMSC dependent as the phenotype was observed after\neffector T cells were adoptively transferred into na�±�¨ve syngeneic mice. Our data suggest that minor\nantigen mismatched BMSCs trigger systemic fibrosis in this autoimmune scleroderma model.\nDOI: 10.7554/eLife.09394.001
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