Core Viewpoint - The study highlights the role of DNASE1L3-expressing dendritic cells in enhancing CD8+ T cell function and improving the efficacy of anti-PD-1/PD-L1 therapies by degrading neutrophil extracellular traps (NETs) [2][3][5]. Group 1: Research Findings - The expression of DNASE1L3 in tumor-infiltrating dendritic cells is positively correlated with better prognosis in cancer patients undergoing anti-PD-1/PD-L1 therapy [5]. - Conditional knockout of DNASE1L3 in dendritic cells leads to accelerated tumor growth and reduced efficacy of anti-PD-L1 therapy due to impaired CD8+ T cell infiltration and function [5]. - Exogenous supplementation of DNASE1L3 enhances CD8+ T cell infiltration into the tumor microenvironment, reduces T cell exhaustion, significantly inhibits tumor growth, and improves responses to anti-PD-L1 therapy [5]. Group 2: Mechanistic Insights - DNASE1L3+ dendritic cells maintain a cytotoxic CD8+ T cell hub by degrading NETs, which inhibit the spatial distribution of CD8+ T cells within tumors [5][8]. - The absence of DNASE1L3 in dendritic cells promotes tumor growth through CD8+ T cell dysfunction [5][8]. Group 3: Implications for Therapy - DNASE1L3 is identified as a promising new target for improving the effectiveness of anti-PD-1/PD-L1 therapies [8].