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KLHL6 tunes T cell fate to boost cancer immunotherapy

A Nature study identifies the E3 ubiquitin ligase KLHL6 as a dual regulator of CD8+ T cell exhaustion and mitochondrial fitness. KLHL6 promotes TOX poly-ubiquitination and degradation, delaying terminal exhaustion, while also restraining excessive mitochondrial fission via the PGAM5–Drp1 axis to maintain T cell metabolism. TCR stimulation downregulates KLHL6, but enforced KLHL6 expression in adoptively transferred T cells enhances anti-tumor and anti-viral responses, highlighting KLHL6 as a clinically actionable target to improve cancer immunotherapy by tuning proteostasis.

17 hours ago•Source: Nature

The Impact of Tumor Heterogeneity on Immunogenicity in Mismatch Repair Deficient Tumors

cancer-immunotherapy

2.84 min•2 years ago

The Impact of Tumor Heterogeneity on Immunogenicity in Mismatch Repair Deficient Tumors

Tumor heterogeneity can impair immunogenicity in mismatch repair deficient (MMRd) tumors, potentially leading to immunotherapy failure. While high tumor mutational burden (TMB) is associated with exceptional immunotherapy responses, some MMRd patients do not experience clinical benefit. Recent research suggests that high intra-tumoral heterogeneity can offset immunogenicity in sporadic MMRd tumors, highlighting the need for further investigation into the mechanisms underlying immunotherapy resistance.

via Nature.com

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KLHL6 tunes T cell fate to boost cancer immunotherapy

The Impact of Tumor Heterogeneity on Immunogenicity in Mismatch Repair Deficient Tumors

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