Immune Escape after Hematopoietic Stem Cell Transplantation (HSCT): From Mechanisms to Novel Therapies

Acute myeloid leukemia (AML) is the most common type of acute leukemia in adults. Recent advances in understanding its molecular basis have opened the way to new therapeutic strategies, including targeted therapies. However, despite an improvement in prognosis it has been documented in recent years...

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Bibliographic Details
Published in:Cancers 2019-12, Vol.12 (1), p.69
Main Authors: Bernasconi, Paolo, Borsani, Oscar
Format: Article
Language:English
Subjects:
Acute myeloid leukemia
Antigens
Chemotherapy
Cytokines
Genes
Hematopoietic stem cells
Histocompatibility antigen HLA
Immune checkpoint
Immune evasion
Immune response
Immunology
Immunotherapy
Inflammation
Leukemia
Lymphocytes
Myeloid leukemia
Review
Risk groups
Stem cell transplantation
Stem cells
Transplants & implants
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Summary:Acute myeloid leukemia (AML) is the most common type of acute leukemia in adults. Recent advances in understanding its molecular basis have opened the way to new therapeutic strategies, including targeted therapies. However, despite an improvement in prognosis it has been documented in recent years (especially in younger patients) that allogenic hematopoietic stem cell transplantation (allo-HSCT) remains the only curative treatment in AML and the first therapeutic option for high-risk patients. After allo-HSCT, relapse is still a major complication, and is observed in about 50% of patients. Current evidence suggests that relapse is not due to clonal evolution, but instead to the ability of the AML cell population to escape immune control by a variety of mechanisms including the altered expression of HLA-molecules, production of anti-inflammatory cytokines, relevant metabolic changes and expression of immune checkpoint (ICP) inhibitors capable of "switching-off" the immune response against leukemic cells. Here, we review the main mechanisms of immune escape and identify potential strategies to overcome these mechanisms.
ISSN:2072-6694
2072-6694
DOI:10.3390/cancers12010069