Myeloid neoplasms (myelodysplastic syndromes, myeloproliferative neoplasms, and acute myeloid leukemias) are characterized by disrupted myelopoiesis encompassing increased apoptosis of bone marrow progenitors, differentiation arrest, and increased proliferation. This results in either peripheral cytopenia (with anemia, bleeding, and infectious risk), or in hyperproliferative phenotype (with splenomegaly, high blood counts, and thrombosis). Although the “first hit” is thought to be a genetic lesion of the hematopoietic stem cell, there is growing attention to the surrounding immunologic niche. Clinically, the immune system disruption is supported by an increased incidence of autoimmune phenomena in myeloid neoplasms, which may worsen the degree of cytopenia (particularly anemia and thrombocytopenia) and respond to immunosuppressive therapy. From a pathogenic point of view, bone marrow hematopoietic stem cells are strongly regulated by the crosstalk with the surrounding microenvironment and its components, including mesenchymal stem and lymphoid cells, and macrophages. Several alterations of these cells have been described in myeloid neoplasms, and it is not clear whether they are cause or consequence of disease development and progression. Furthermore, niche disruption might sustain pancytopenia and promote the accumulation of clonal molecular alterations that lead to leukemic evolution. Finally, immunologic alterations might in turn be potential targets for novel biologic drugs.
In this Research Topic on "immunologic mechanisms of myeloid neoplasms," we will focus on the immune aspects of pathogenesis, course, complications, and treatment of myelodysplastic syndromes, myeloproliferative neoplasms, and acute myeloid leukemia. This would include studies showing the "failure" of immune surveillance involved in myeloid disease pathogenesis, on the development of autoimmune complications of the diseases themselves and their treatments (including hematopoietic stem cell transplant), and on the "old and novel immunotherapies" used in hematology. Studies addressing the interplay between clonal myelopoiesis and the immune system, as well as aimed at demonstrating a clonal lymphopoiesis or genetic lesions involving the immune system in myeloid neoplasms would highly help to meet the goal.
Original Articles, Case Reports, Reviews, and Mini-Reviews will be welcomed, provided they aim to clarify the role of the immune system in myeloid neoplasms. Studies on inflammation and thrombosis will also be considered, as well as those dealing with rarer entities such as mast-cell disorders, paroxysmal nocturnal hemoglobinuria, and aplastic anemia. The following topics will be considered:
? The role of the immune system in the pathogenesis of myeloid neoplasms (including chronic infection/inflammation and autoimmunity as triggers for neoplastic transformation)
? Immune mechanisms modulating the clinical course of myeloid neoplasms, including leukemic evolution and development of complications (autoimmune complications, infections, thrombosis)
? Mechanisms involved in the interplay between the immune system and the neoplastic hematopoietic stem cell (including studies on the alteration of the niche, the role of lymphoid, mesenchymal, and monocyte/macrophage cells, etc.)
? Molecular studies on genetic lesions involving both the myeloid cells and the immunologic cells, including those on clonal hematopoiesis and the contribution of the immune system to clone selection
? How therapies used for myeloid neoplasms alter the immune system (including studies on infection complications after chemotherapy, autoimmune complications after biologic drugs, hematopoietic stem cell transplant, and microbiome)
? The immune system as a therapeutic target in myeloid neoplasms (all studies involving old and new drugs with immunomodulatory properties)
Myeloid neoplasms (myelodysplastic syndromes, myeloproliferative neoplasms, and acute myeloid leukemias) are characterized by disrupted myelopoiesis encompassing increased apoptosis of bone marrow progenitors, differentiation arrest, and increased proliferation. This results in either peripheral cytopenia (with anemia, bleeding, and infectious risk), or in hyperproliferative phenotype (with splenomegaly, high blood counts, and thrombosis). Although the “first hit” is thought to be a genetic lesion of the hematopoietic stem cell, there is growing attention to the surrounding immunologic niche. Clinically, the immune system disruption is supported by an increased incidence of autoimmune phenomena in myeloid neoplasms, which may worsen the degree of cytopenia (particularly anemia and thrombocytopenia) and respond to immunosuppressive therapy. From a pathogenic point of view, bone marrow hematopoietic stem cells are strongly regulated by the crosstalk with the surrounding microenvironment and its components, including mesenchymal stem and lymphoid cells, and macrophages. Several alterations of these cells have been described in myeloid neoplasms, and it is not clear whether they are cause or consequence of disease development and progression. Furthermore, niche disruption might sustain pancytopenia and promote the accumulation of clonal molecular alterations that lead to leukemic evolution. Finally, immunologic alterations might in turn be potential targets for novel biologic drugs.
In this Research Topic on "immunologic mechanisms of myeloid neoplasms," we will focus on the immune aspects of pathogenesis, course, complications, and treatment of myelodysplastic syndromes, myeloproliferative neoplasms, and acute myeloid leukemia. This would include studies showing the "failure" of immune surveillance involved in myeloid disease pathogenesis, on the development of autoimmune complications of the diseases themselves and their treatments (including hematopoietic stem cell transplant), and on the "old and novel immunotherapies" used in hematology. Studies addressing the interplay between clonal myelopoiesis and the immune system, as well as aimed at demonstrating a clonal lymphopoiesis or genetic lesions involving the immune system in myeloid neoplasms would highly help to meet the goal.
Original Articles, Case Reports, Reviews, and Mini-Reviews will be welcomed, provided they aim to clarify the role of the immune system in myeloid neoplasms. Studies on inflammation and thrombosis will also be considered, as well as those dealing with rarer entities such as mast-cell disorders, paroxysmal nocturnal hemoglobinuria, and aplastic anemia. The following topics will be considered:
? The role of the immune system in the pathogenesis of myeloid neoplasms (including chronic infection/inflammation and autoimmunity as triggers for neoplastic transformation)
? Immune mechanisms modulating the clinical course of myeloid neoplasms, including leukemic evolution and development of complications (autoimmune complications, infections, thrombosis)
? Mechanisms involved in the interplay between the immune system and the neoplastic hematopoietic stem cell (including studies on the alteration of the niche, the role of lymphoid, mesenchymal, and monocyte/macrophage cells, etc.)
? Molecular studies on genetic lesions involving both the myeloid cells and the immunologic cells, including those on clonal hematopoiesis and the contribution of the immune system to clone selection
? How therapies used for myeloid neoplasms alter the immune system (including studies on infection complications after chemotherapy, autoimmune complications after biologic drugs, hematopoietic stem cell transplant, and microbiome)
? The immune system as a therapeutic target in myeloid neoplasms (all studies involving old and new drugs with immunomodulatory properties)
