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. 2020 Mar 20;11:492. doi: 10.3389/fimmu.2020.00492

Figure 1.

Figure 1

Potential hypotheses explaining hyperprogression. Ten potential mechanisms that may be responsible for hyperprogression following administration of immunotherapies. (A) HPD is not caused by immunotherapies but it is a consequence of adverse prognostic profiles. (B) Activation of oncogenic pathways caused by PD-1/PD-L1 axis blockade. (C) Non-immunogenic subclones resistant to chemotherapy develop very quickly following the cessation of chemotherapy. (D) The TH17 axis causes increased inflammation following immunotherapy administration. (E) Tumor associated DCs contribute to immunosuppression of the microenvironment after blocking of the PD-1/PD-L1 axis. (F) PD1/PD-L1 blockade activates ILC3 which enhances immunosuppression by protumoral interleukins. (G) Blocking of PD-1 activates Treg PD1+ which induces suppression of Teff. (H) Activation, by PD-1/PD-L1 axis blocking, of M2-like PD-L1+ cells which promote tumor growth directly and indirectly by expansion of protumoral cells. (I) Fc receptor of anti-PD-1 enhances tumor growth by recruitment of M2-like cells. (J) gMDSC following immunotherapies induces immunosuppression by release metabolites which suppress antitumor cells.