Induction of Graft versus Host Disease in SCID Mice by MRL/lpr Cell Transfer

Fraziano, Maurizio; Montesano, Carla; Sammarco, Innocenzo; Cesare, Silvia Di; Caroleo, Maria Cristina; Mattei, Maurizio; Cannata, Stefano; Poccia, Fabrizio; Bellavia, A; Salerno, Alfredo; Colizzi, Vittorio

doi:10.1006/clin.1994.1085

Cited by 4 publications

(2 citation statements)

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“…Supernatant levels of IL-17 of T-SNTSC and T-hBMMSC cultures were markedly lower than those of T-MRL/lpr ( Figure 4C). We transplanted these T-cells into SCID mice (Fraziano et al, 1994) and assessed in vivo survival damage. The transplantation of T-SNTSC-and T-hBMMSC extended the shortened lifespan of T-MRL/lpr-transplanted mice (Fig.…”

Section: Sntsc Transplantation Suppresses Hyperimmunoreactivity Of T-mentioning

confidence: 99%

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Immune Therapeutic Potential of Stem Cells from Human Supernumerary Teeth

et al. 2013

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Discoveries of immunomodulatory functions in mesenchymal stem cells (MSCs) have suggested that they might have therapeutic utility in treating immune diseases. Recently, a novel MSC population was identified from dental pulp of human supernumerary teeth, and its multipotency characterized. Herein, we first examined the in vitro and in vivo immunomodulatory functions of human supernumerary tooth-derived stem cells (SNTSCs). SNTSCs suppressed not only the viability of T-cells, but also the differentiation of interleukin 17 (IL-17)-secreting helper T (Th17)-cells in in vitro co-culture experiments. In addition, systemic SNTSC transplantation ameliorated the shortened lifespan and elevated serum autoantibodies and nephritis-like renal dysfunction in systemic lupus erythematosus (SLE) model MRL/lpr mice. SNTSC transplantation also suppressed in vivo increased levels of peripheral Th17 cells and IL-17, as well as ex vivo differentiation of Th17 cells in MRL/lpr mice. Adoptive transfer experiments demonstrated that SNTSC-transplanted MRL/lpr mouse-derived T-cell-adopted immunocompromised mice showed a longer lifespan in comparison with non-transplanted MRL/lpr mouse-derived T-cell-adopted immunocompromised mice, indicating that SNTSC transplantation suppresses the hyper-immune condition of MRL/lpr mice through suppressing T-cells. Analysis of these data suggests that SNTSCs are a promising MSC source for cell-based therapy for immune diseases such as SLE.

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Section: Sntsc Transplantation Suppresses Hyperimmunoreactivity Of T-mentioning

confidence: 99%

“…Supernatant levels of IL-17 of T-SNTSC and T-hBMMSC cultures were markedly lower than those of T-MRL/lpr (Figure 4C). We transplanted these T-cells into SCID mice (Fraziano et al, 1994)…”

Section: Sntsc Transplantation Suppresses Hyperimmunoreactivity Of T-cells Especially Th17 Cells In Mrl/lpr Micementioning

confidence: 99%

Immune Therapeutic Potential of Stem Cells from Human Supernumerary Teeth

et al. 2013

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Constitutive activation of the Fas ligand gene in mouse lymphoproliferative disorders.

et al. 1995

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Mice homozygous for lpr (lymphoproliferation) or gld (generalized lymphoproliferative disease) develop lymphadenopathy and splenomegaly and suffer from autoimmune disease. The lpr mice have a defect in a cell‐surface receptor, Fas, that mediates apoptosis, while gld mice have a mutation in the Fas ligand (FasL). Northern hybridization with the FasL cDNA as probe indicated that the cells accumulating in lpr and gld mice abundantly express the FasL mRNA without stimulation. By means of in situ hybridization and immunohistochemistry, we identified the cells expressing the FasL mRNA as CD4‐CD8‐ double negative T cells. The T cells from lpr mice were specifically cytotoxic against Fas‐expressing cells. Since FasL is normally expressed in activated mature T cells these results indicate that the double negative T cells accumulating in lpr and gld mice are activated once, and support the notion that the Fas/FasL system is involved in activation‐induced suicide of T cells. Furthermore, the graft‐versus host disease caused by transfer of lpr bone marrow to wild‐type mice can be explained by the constitutive expression of the FasL in lpr‐derived T cells.

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