All articles tagged with #pd l1
Ultra-accurate sequencing shows somatic mutations in immune cells, especially B cells, can disable immune brakes and drive thyroid autoimmune diseases (Hashimoto’s and Graves’). This polyclonal evolution suggests a new mechanism beyond inheritance and hints at precision therapies that target mutant cell clones rather than broad immune suppression.
Using whole-exome sequencing and NanoSeq, researchers detected numerous B-cell clones with loss-of-function mutations in HVEM (TNFRSF14) and PD-L1 (CD274) in inflamed autoimmune thyroid tissue. In highly inflamed samples there are tens to hundreds of independent mutant clones, often with multiple hits and occasional biallelic loss, localizing to self-reactive B cells and supporting a model in which somatic immune-regulatory mutations contribute to thyroid autoimmunity.
Cancer cells release PD-L1–containing small extracellular vesicles that dampen immune attacks; the PD-L1 is sorted into these vesicles via a UBL3-driven modification at cysteine 272. Statins inhibit this modification, reducing PD-L1 packaging into vesicles and potentially enhancing responses to PD-1/PD-L1 inhibitors; early patient data show statin users have fewer PD-L1–positive vesicles, suggesting statins could be added to immunotherapy regimens to improve outcomes.
Researchers found that cancer cells load the immune-inhibiting protein PD-L1 into tiny extracellular vesicles via the protein UBL3, helping tumors suppress immune responses. Statins block this UBL3-driven modification, reducing PD-L1 cargo and potentially improving responses to immune checkpoint inhibitors, with supporting evidence from non-small cell lung cancer patients showing fewer PD-L1–containing vesicles in those taking statins.