Conclusion
In conclusion, the tumor immune microenvironment of EGFR mutated NSCLC is different from that of non-mutated NSCLC, which is one of the reasons why EGFR mutated NSCLC is a poor response to ICI. The tumor immune microenvironment of EGFR mutated NSCLC also changes during the treatment of EGFR-TKIs. The tumor immune microenvironment of EGFR-TKIs resistance can be summarized into three points:1. Comparing with EGFR-TKIs sensitive tumor, there are more immunosuppressive cells and fewer immune activated cells in EGFR-TKIs resistant tumor and the tumor microenvironment is an immunosuppressive state;2. Tumor cells and immunosuppressive cells secrete many immune negative regulatory factors, inhibit the recognition and presentation of tumor antigen and the antitumor effect of immune cells, resulting in immune escape;3.EGFR-TKIs resistant tumor appears EMT. The above three points interact with each other to form a signal regulatory network, which together leads to EGFR-TKIs resistance. Inhibiting one of them can not fundamentally reverse the EGFR-TKIs resistance. Therefore, future research on reversing EGFR-TKIs resistance needs to invent pan targeted drugs that inhibit the key points of the signal regulatory network, change immune cell infiltration, change immune regulatory factors and reverse EMT, and finally reverse EGFR TKIs resistance.