Fig. 1

DC cross-talk within the TME. cDC1s and cDC2s recruit cytotoxic T lymphocytes (CTL) to the TME by secreting the chemokines CXCL9 and CXCL10, leading to an anti-tumor response. pDCs promoting the differentiation of Treg are associated with unfavorable clinical outcomes. LAMP3⁺ DCs, potentially originating from cDC1s and cDC2s, possess the capacity to migrate to lymph nodes. cDC1-derived LAMP3⁺ DCs notably express high levels of BTLA and drive Treg differentiation, whereas cDC2-derived LAMP3⁺ DCs exhibit elevated CCL17 expression, attracting Tregs to tumors. IL-12 expression in LAMP3⁺ DCs is downregulated by IL-4; however, blocking IL-4 augments IL-12 production and expands the population of IFNγ⁺ CD8⁺ T effector cells. LAMP3⁺ DCs inhibit T cell activation via CTLA4 and engage in interactions with Treg cells via CD80/CD86