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We next analyzed the effects of BMS1166 on the post-translational processing of PD-L1 using cells expressing a GFP-tagged PD-L1 (PD-L1-GFP). We found that the PD-L1-GFP was trapped in ER after BMS1166 treatment (Figure 5(c,d)). There was no PD-L1-GFP to be found on the cell surface or in the Golgi, which was labeled by the anti-GM130 antibody,30 demonstrating that BMS1166 prevented the newly-synthesized PD-L1 from transporting into Golgi to undergo further glycosylation.31

Using the PC9/PD-L1-Jurkat/PD-1 coculture assay, we found that a small-molecule BMS1166, designed and synthesized by Bristol-Myers Squibb to disrupt the PD-L1-PD-1 interaction, blocked the coculturing-induced PD-1 degradation by an unexpected mechanism. We provide sufficient evidences to suggest that the binding of BMS1166 to PD-L1 blocked the post-translational processing of PD-L1, preventing it from directly interacting with PD-1. BMS1166 retained the newly synthesized and partially glycosylated PD-L1 in the ER and prevented its exporting from ER to Golgi and further glycosylation and maturation.

CVE 2019-1166: This vulnerability allows attackers to bypass the MIC (message integrity code) protection on NT LAN Manager (NTLM) authentication and thereby modify any field in the NTLM message flow, including the signing requirement. This bypass allows attackers to relay authentication attempts that have successfully negotiated signing onto another server while tricking the server into ignoring the signing requirement. All servers that do not enforce signing are vulnerable to this attack. This is the second MIC bypass vulnerability found by the Preempt (now CrowdStrike) team. 59ce067264


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