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In EAE, as in human MS, there are selective alterations in TJ proteins, including a notable loss of claudin-3, while other key TJs such as ZO-1, occludin, and claudin-5 are also significantly disrupted, contributing to barrier breakdown and neuroinflammation [135, 136]
For example, cotargeting IL-6/JAK/STAT3 signaling and the PD-1/PD-L1 axis may overcome immune resistance in PD-L1 high tumors with elevated IL-6
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