Immune surveillance mechanisms comprising of adaptive and innate immune systems are naturally designed to eliminate AML development. However, leukemic cells apply various immune evasion mechanisms to deviate host immune responses… Click to show full abstract
Immune surveillance mechanisms comprising of adaptive and innate immune systems are naturally designed to eliminate AML development. However, leukemic cells apply various immune evasion mechanisms to deviate host immune responses resulting tumor progression. One of the recently well-known immune escape mechanisms is over-expression of immune checkpoint receptors and their ligands. Introduction of blocking antibodies targeting co-inhibitory molecules achieved invaluable success in tumor targeted therapy. Moreover, several new co-inhibitory pathways are currently studying for their potential impacts on improving anti-tumor immune responses. Although immunotherapeutic strategies based on the blockade of immune checkpoint molecules have shown promising results in a number of hematological malignances, their effectiveness in AML patients showed less remarkable success. This review discusses current knowledge about the involvement of co-inhibitory signaling pathways in immune evasion mechanisms of AML and potential application of immune checkpoint inhibitors for targeted immunotherapy of this malignancy.
               
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