TIGIT blockade enhances tumor response to radiotherapy via a CD103 + dendritic cell-dependent mechanism

• DOI: 10.1007/s00262-022-03227-z
• Publication Date: 2022-07-06T17:03:10Z
• Authors: Kaikai Zhao; Liyang Jiang; Youjiao Si; Shujie Zhou; Zhaoqin Huang; Xiangjiao Meng
• Keywords: TIGIT

Abstract Blockade of the T cell immunoreceptor with immunoglobulin and tyrosine-based inhibitory motif domain (TIGIT) can enhance innate adaptive tumor immunity radiotherapy (RT) anti-tumor immunity. However, our data suggest that TIGIT-mediated immune suppression may be an impediment to such goals. Herein, we report on synergistic effects RT combined anti-TIGIT therapy mechanism their interaction. Treatment efficacy was assessed by measuring primary secondary growth, survival, memory capacity. The function CD103 + dendritic cells (DCs) under treatment in wild-type BATF3-deficient (BATF3 −/− ) mice. FMS-like tyrosine kinase 3 ligand (Flt3L) used confirm role DCs therapy. TIGIT upregulated following both esophageal squamous carcinoma patients mouse models. Administration antibody enhanced through a CD8 cell-dependent mechanism. It observed synergistically accumulation tumor-infiltrating DCs, which activated cells. combination negated BATF3 model. were required promote Additionally, Flt3L response blockade. Our study demonstrated blockade responses via (dependent DCs), suggesting clinical potential targeting pathway expanding RT.