AIM: To investigate the expression of Th22 cells and related cytokines in colorectal cancer(CRC) tissues, and the probably mechanism.METHODS: CRC tumor and paratumor tissues were collected to detect the expression levels of Th22 cells and of related cytokines by immunohistochemistry, flow cytometry and real-time quantitative polymerase chain reaction(RT-q PCR).Interleukin(IL)-22 alone or with a STAT3 inhibitor was co-cultured with RKO cells in vitro to study the effects of IL-22 on colon cancer cells.IL-22 alone or with a STAT3 inhibitor was injected into a BALB/c nude mouse model with subcutaneously transplanted RKO cells to study the effects of IL-22 on colon cancer growth.RESULTS: The percentage of Th22 cells in the CD4+ T subset was significantly higher in tumor tissues compared with that in paratumor tissues(1.47% ± 0.083% vs 1.23% ± 0.077%, P < 0.05) as determined by flow cytometry.RT-qP CR analysis revealed that the m RNA expression levels of IL-22, aryl hydrocarbon receptor, CCL20 and CCL22 were significantly higher in tumor tissues compared with those in paratumor tissues.CCL27 mR NA also displayed a higher expression level in tumor tissues compared with that in paratumor tissues; however, these levels were not significantly different(2.58 ± 0.93 vs 2.30 ± 0.78, P > 0.05).IL-22 enhanced colon cancer cell proliferation in vitro and displayed anti-apoptotic effects; these effects were blocked by adding a STAT3 inhibitor.IL-22 promoted tumor growth in BALB/c nude mice; however, this effect was reversed by adding a STAT3 inhibitor.CONCLUSION: Th22 cells that accumulate in CRC may be associated with the chemotactic effect of the tumor microenvironment.IL-22 is associated with CRC development, most likely via STAT3 activation.