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GM-CSF induces bone marrow precursors of NOD mice to skew into tolerogenic dendritic cells that protect against diabetes

机译：GM-CSF诱导NOD小鼠的骨髓前体偏向耐受糖尿病的耐受性树突状细胞

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We have reported that GM-CSF treatment of NOD mice suppressed diabetes by increasing the number of tolerogenic dendritic cells (tDCs) and Tregs in the periphery. Here, we have investigated whether GM-CSF acted on NOD bone marrow DCs precursors to skew their differentiation to tDCs. DCs were generated from the bone marrow of GM-CSF-treated (GM.BMDCs) and PBS-treated (PBS.BMDCs) NOD mice and were assessed for their ability to acquire tolerogenic properties. Upon LPS stimulation, GM.BMDCs became fully mature, expressed high levels of PD-L1 and produced more IL-10 and less IL-12p70 and IFN-γ than PBS.BMDCs. In addition, LPS-stimulated GM.BMDCs possessed a reduced capacity to activate diabetogenic CD8+ T cells in a PD-1/PD-L1-dependent manner. A single injection of LPS-stimulated GM.BMDCs in NOD mice resulted in long-term protection from diabetes, in contrast to LPS-stimulated PBS.BMDCs. Our results showed that GM-CSF-treatment acted on bone marrow precursors to skew their differentiation into tDCs that protected NOD mice against diabetes.
机译：我们已经报道了GM-CSF对NOD小鼠的治疗通过增加外周耐受性树突状细胞（tDCs）和Tregs的数量来抑制糖尿病。在这里，我们研究了GM-CSF是否作用于NOD骨髓DCs前体以使其分化为tDCs。 DCs是由GM-CSF处理过的（GM.BMDCs）和PBS处理过的（PBS.BMDCs）NOD小鼠的骨髓产生的，并评估了它们获得致耐受性的能力。 LPS刺激后，GM.BMDCs变得完全成熟，表达高水平的PD-L1，与PBS.BMDCs相比，产生更多的IL-10和更少的IL-12p70和IFN-γ。此外，LPS刺激的GM.BMDC具有降低的以PD-1 / PD-L1依赖性方式激活造糖尿病CD8 + T细胞的能力。与LPS刺激的PBS.BMDCs相反，在NOD小鼠中单次注射LPS刺激的GM.BMDCs可以长期预防糖尿病。我们的结果表明，GM-CSF处理可作用于骨髓前体，使其分化为tDCs，从而保护NOD小鼠免于糖尿病。

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