Abstract
The recent use of T cell-based cancer immunotherapies, such as adoptive T-cell transfer and checkpoint blockade, yields increasing clinical benefit to patients with different cancer types. However, decrease of MHC...
Highlights
Major histocompatibility complex (MHC) class I display is a fundamental defense mechanism enabling CD8+ T lymphocytes to identify and kill infected or transformed cells
It recently became clear that the nucleotide-binding oligomerization domain (NOD)-like receptor (NLR) family member NLRC5 (NLR caspase recruitment domain containing protein 5) is a key transcriptional regulator of the MHC class I pathway [3,4,5,6,7]
Nlrc5 knockout mouse models demonstrated the crucial role of this NOD-like receptor (NLR) to maintain high MHC class I expression in several cell types and most prominently in lymphocytes [4,5,6,7]
Summary
Major histocompatibility complex (MHC) class I display is a fundamental defense mechanism enabling CD8+ T lymphocytes to identify and kill infected or transformed cells. Nlrc5 knockout mouse models demonstrated the crucial role of this NLR to maintain high MHC class I expression in several cell types and most prominently in lymphocytes [4,5,6,7]. Both in human and mouse, NLRC5 has a very focused transcriptional regulatory activity, controlling expression of classical and selected non-classical MHC class I genes, and few genes coding for APM proteins [3, 5].
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