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This study confirmed the pathogenicity of the Y139C heterozygous mutation, providing supporting evidence for CTLA-4 haploinsufficiency and revealed that compensatory mechanisms arise in response to compromised trans-endocytosis.
A conceptual framework for understanding HDL-centered cholesterol metabolism in ccRCC is provided and potential metabolic vulnerabilities for therapeutic targeting are highlighted and outlined.
This work demonstrates that GRP75 deficiency disrupts CD8+ T cell fate, leading to defective T cell homeostasis and impaired memory differentiation, and establishes GRP75 as a pivotal mitochondrial checkpoint that coordinates metabolic state and functional fate in CD8+ T cells.
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