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Colony-stimulating factor 1 receptor (CSF-1R) acts as the receptor for colony stimulating factor 1, a cytokine that controls the production, differentiation, and function of macrophages. Prior studies showed cancer patients harboring germline  CSF1R  c.1085A>G genetic variant had better survival. Here, primary tumor samples from a stage III colorectal cancer (CRC) cohort were analyzed by a targeted gene expression assay containing 395 immune-related genes to study the immune mechanism underlying the different outcomes. CRC patients with  CSF1R  c.1085 genotype A_G had a better disease-free and overall survival than those with  CSF1R  genotype A_A. Compared to the group of patients without  CSF1R  variant, higher  CD40LG  expression, a surface marker of T cells, was found in the tumor tissues of patients with  CSF1R  c.1085 variant. In parallel with the higher  CD40LG  gene expression, immunofluorescent staining also showed more CD3 + CD40L +  T cell infiltrates in tumors with  CSF1R  c.1085 genotype A_G. Moreover, higher IL-2 expression, known to be regulated by CD40 pathway, was also observed in tumors with  CSF1R  c.1085 genotype A_G than genotype A_A. Higher IL-2 expression generated by the interaction of CD40 ligand and CD40 between T cells and macrophages with  CSF1R  c.1085A>G variant is the potential mechanism explaining the different outcomes.

CD40 Pathway and IL-2 Expression Mediate the Differential Outcome of Colorectal Cancer Patients with Different CSF1R c.1085 Genotypes