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For example, the crystal structure of the full-length GSDMD has revealed the mechanism of auto-inhibition of the inactive full-length protein (Figure 4B) [167]

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This comparison synthesizes published clinical trial data into a single reference

Taken together, the above observations suggest that B cells might play a key upstream role in MS pathogenesis, and quite unexpectedly, could be stimulated to upregulate machinery unrelated to their traditional immune functions (Lisak et al., 2012, 2017)