布鲁顿酪氨酸激酶抑制通过阻断抑制性BDCA-2途径增强浆细胞样树突状细胞中Toll样受体7介导的α干扰素产生。
BTK-Inhibition Enhances TLR-7-Mediated Interferon-Alpha Production in pDCs by Blocking the Inhibitory BDCA-2 Pathway.
作者信息
Ceglarek Laura, Gerhards Ramona, Boldrini Vinicius, Wichmann Christian, Peters Anneli, Meinl Edgar
机构信息
Institute of Clinical Neuroimmunology, Biomedical Center and University Hospital, Ludwig-Maximilians-Universität München, Munich, Germany.
Center for Human Immunology, University of Zurich, Zurich, Switzerland.
出版信息
Eur J Immunol. 2025 Feb;55(2):e202450985. doi: 10.1002/eji.202450985.
In pDCs, BTK-inhibition (BTKi) blocks the IFN-α production via TLR-9, but not via TLR-7. Upon TLR-7 stimulation, BTKi enhances the production of IFN-α by blocking the inhibitory BDCA-2 pathway. This might explain partially the failure of BTKi in SLE and is of interest for BTKi trials in multiple sclerosis.
在浆细胞样树突状细胞（pDCs）中，布鲁顿酪氨酸激酶抑制（BTKi）可通过Toll样受体9（TLR-9）阻断Ⅰ型干扰素（IFN-α）的产生，但不能通过Toll样受体7（TLR-7）。在TLR-7刺激下，BTKi通过阻断抑制性的血树突状细胞抗原2（BDCA-2）途径增强IFN-α的产生。这可能部分解释了BTKi在系统性红斑狼疮（SLE）治疗中失败的原因，并且对于在多发性硬化症中进行BTKi试验具有重要意义。
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