JAK inhibition (JAKi) is effective in seronegative spondyloarthropathy (SpA) spectrum disorders, but Tyk2 inhibition failed in SpA spectrum ulcerative colitis, and tofacitinib showed minimal benefit in Crohn disease, which highlights the complex role for JAK/STAT signaling in different inflammatory processes. In this study, we investigated whether JAKi might paradoxically activate entheseal innate immunity and aimed to identify the key regulatory cytokines involved in this process.

中文翻译：

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JAK1 和 Tyk2 抑制剂通过白细胞介素 10 拮抗作用反常激活附着点髓系细胞

JAK 抑制（JAKi）对血清阴性脊柱关节病（SpA）谱系疾病有效，但 Tyk2 抑制在 SpA 谱溃疡性结肠炎中失败，托法替尼在克罗恩病中获益微乎其微，这凸显了 JAK/STAT 信号传导在不同炎症过程中的复杂作用。在这项研究中，我们调查了 JAKi 是否可能自相矛盾地激活附着点先天免疫，并旨在确定参与这一过程的关键调节细胞因子。