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.