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T.et al (2004)

Different from intracellular MHC class II, which forms a signaling complex with Btk and CD40 to sustain LPS-induced Btk phosphorylation and enhance MyD88/TRIF-dependent cytokine production [34], constitutively expressed membrane MHC-I suppresses TLR signaling via Src-mediated phosphorylation of their intracellular domains, recruiting Fps and SHP-2 to inhibit TRAF6-dependent TLR signaling, thereby protecting mice from sepsis [35]

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KPV addresses any inflammatory component that may be contributing even without an identified inflammatory cause