IL22 overexpression

P=N/A, N=60, Active, not recruiting, NHS Lothian | Unknown status --> Active, not recruiting | Trial completion date: Feb 2022 --> Aug 2025 | Trial primary completion date: Feb 2022 --> Aug 2025

Overall, we show that IL-22/AKT signaling increases MASTL expression to promote cell survival and proliferation. Further, CAIX stabilizes MASTL by associating with it in response to IL-22 stimulation.

We demonstrated that EA affected apoptosis by regulating the IL-22/JAK2-STAT3 pathway in NP cells and reducing inflammatory factors in the CIDD rat model. The results extend our knowledge of the mechanisms of action underlying the effects of EA as a potential treatment approach for CS in clinical practice.

Conclusions IL-22 expression in lung cancer tissue of earlystage NSCLC was significantly higher in men, lung adenocarcinoma, current smokers and showed a trend to be higher in NSCLC patients with concomitant COPD compared to NSCLC without COPD. Our findings indicate that IL-22 may represent a promising therapeutic target for NSCLC.

IL-22-producing iNKT cells promoting metastasis were tissue resident, as demonstrated by parabiosis. Thus, IL-22 may present a therapeutic target for prevention of metastasis.

T helper cell 22 are abundant in Hepatitis B Virus-related hepatocellular carcinoma tissue, and the main cytokine interleukin 22 produced by Th22 cells is closely related to the initiation and development of HCC...Our data suggests that HBV induces host Th22 cells to overexpress IL-22, which in turn triggers over-activation of STAT3 and its downstream signaling proteins to promote HCC progression. The online version contains supplementary material available at 10.1007/s10616-021-00517-9.

In the present study, exogenous IL-22 was found to upregulate PD-L1 expression via the signal transducer and activator of transcription 3 signaling pathway in human colon cancer cells (DLD-1 and primary colon cancer cells). The results of the present study revealed a novel regulatory mechanism of PD-L1 expression in colon cancer, which provides a theoretical basis for decreasing the immune tolerance of colon cancer via IL-22 overexpression.