The interactions between the immune system and the tumor cells occur through complex events that lead to tumor eradication or immune evasion by cancer. Recently, the prognostic role of Myeloid derived suppressor cells (MDSC) accumulation has been documented for some hematological malignancies where they correlates with disease progression and persistence of minimal residual disease. We first evaluated the change of MDSC frequency in hematological patients during therapy founding a significant correlation between the number of persistent monocytic-MDSC and major molecular response (MMR) value in chronic myeloid leukemia patients treated with dasatinib. Moreover, our data demonstrated that tumor cells, through the release of soluble factors and exosomes, are able to expand monocytic-MDSC, creating an immunotolerant environment that results in T cell anergy and facilitates tumor growth. In addition, cancer cells are also able to promote immune dysfunction in MSC with their consequent commitment, via TLR4 signaling, toward an activated status promoting immune escape through the polarization of neutrophils in immunosuppressive cells.
IMMUNE ESCAPE MECHANISMS IN HEMATOLOGICAL DISEASES: ROLE OF THE MYELOID DERIVED SUPPRESSOR CELLS AND TUMOR MICROENVIRONMENT
GIALLONGO, CESARINA
2017
Abstract
The interactions between the immune system and the tumor cells occur through complex events that lead to tumor eradication or immune evasion by cancer. Recently, the prognostic role of Myeloid derived suppressor cells (MDSC) accumulation has been documented for some hematological malignancies where they correlates with disease progression and persistence of minimal residual disease. We first evaluated the change of MDSC frequency in hematological patients during therapy founding a significant correlation between the number of persistent monocytic-MDSC and major molecular response (MMR) value in chronic myeloid leukemia patients treated with dasatinib. Moreover, our data demonstrated that tumor cells, through the release of soluble factors and exosomes, are able to expand monocytic-MDSC, creating an immunotolerant environment that results in T cell anergy and facilitates tumor growth. In addition, cancer cells are also able to promote immune dysfunction in MSC with their consequent commitment, via TLR4 signaling, toward an activated status promoting immune escape through the polarization of neutrophils in immunosuppressive cells.File | Dimensione | Formato | |
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https://hdl.handle.net/20.500.14242/76616
URN:NBN:IT:UNICT-76616