The incidence of malignant blood diseases has been steadily increasing over past decades. Unlike many other types of malignant neoplasms, blood cancers often occur at a young age, being also the main cause of death among all hematopoietic disorders in pediatric patients. Mutation events in hematopoietic stem cells are the cause of blood cancers which subsequently lead to increasimg number of tumor clones and displacement of healthy cells in the niches they occupy thus leading to a number of changes in blood and bone marrow, including irreversible ones. The aim of this study was to assess the subpopulation composition of pluripotent hematopoietic stem cells in patients with blood cancers and healthy donors. The study included patients with blood cancers (n = 13), including acute lymphoblastic leukemia (ALL; n = 3), acute myeloid leukemia (AML; n = 3), and multiple myeloma (MM; n = 7), as well as healthy donors (n = 4). The phenotypic composition of hematopoietic CD34+CD38- pluripotent cells was assessed by flow cytometry using the following monoclonal antibodies: CD34 APC (BioLegend, USA), CD38 PE-Cy7 (ElabScience, China), CD45RA PerCP (ElabScience, China), CD90 APC-Cy7 (Cloud-Clone Corp., USA), Lin- (cocktail CD3/14/16/19/20/56) FITC (BioLegend, USA). The following populations were assessed: hematopoietic stem cells (Lin-CD34+CD38-CD45RA-CD90+) and pluripotent progenitors (Lin-CD34+CD38-CD45RA-CD90-). In patients with hemoblastoses, the relative number of cells with Lin-CD34+CD38-CD45RA-CD90+ phenotype proved to be increased, thus corresponding to hematopoietic stem cells, but not pluripotent progenitor cells. At the same time, the number of pluripotent progenitor cells tended to decrease in acute myeloid leukemia. We have observed some changes in the subpopulation composition of pluripotent hematopoietic stem cells in patients with blood cancers, when compared with healthy donors.

This study assessed the expression of NKG2 family receptors (NKG2A, NKG2C, NKG2D) on cytotoxic T lymphocytes and NK cells from peripheral blood of patients with multiple myeloma (MM) compared to healthy donors. The relevance of this work is due to the important role of the HLA-E/NKG2 axis in the mechanisms of tumor immune evasion in MM, as well as the potential for therapeutic blockade of these receptors. The study included 10 patients with MM (stage II-III according to Durie–Salmon, in remission) and 9 conditionally healthy donors. Flow cytometry was used to determine the relative abundance of NK cell subpopulations (CD16-CD56+, CD16+CD56+, CD16+CD56-) and CD3+CD4- cytotoxic T lymphocytes expressing NKG2A, NKG2C, and NKG2D. It was found that, compared to donors, MM patients had a significantly higher proportion of NKG2A+ cells among mature CD16+CD56+ NK cells (median 23.8% vs. 7.5%) and among CD16+CD56- NK cells (10.7% vs. 2.1%). At the same time, the proportion of CD3+CD4- cytotoxic T lymphocytes expressing the activating receptor NKG2C was reduced in MM (1.9% vs. 4.6% in donors). The relative abundance of cells expressing NKG2D did not differ between groups for either NK cells or T lymphocytes. These data indicate a shift in balance toward predominance of the inhibitory receptor NKG2A in the NK cell compartment and a reduction of the activating receptor NKG2C in the T cell compartment in multiple myeloma. This may reflect suppression of adaptive cellular immunity and contribute to tumor immune evasion. Thus, the HLA-E/NKG2 axis represents a promising target for further study of the immunopathogenesis of hematologic malignancies and for the development of immunotherapeutic approaches aimed at restoring the function of effector lymphocytes.

Non-Hodgkin lymphomas (NHL) are a heterogeneous group of lymphoproliferative diseases associated with treatment refractoriness and frequent relapses, requiring a search for new pathogenetic mechanisms and prognostic markers. The microenvironment plays a key role in tumor progression where immune cells may either eliminate malignant cells, or promote their survival and dissemination. Innate lymphoid cells (ILCs) and natural killer (NK) cells are components of the innate immune system that can both enhance antitumor response and induce immunosuppression. The objective of our work was to study the phenotypic characteristics of innate lymphoid cell subpopulations (ILC1, ILC2, ILC3) and NK cells (CD16+CD56+, CD16+CD56-, CD16-CD56+) in patients with NHL compared to healthy donors. The study included 7 patients with B cell non-Hodgkin's lymphomas (mean age 44.0±17.6) in complete or partial remission, treated by standard rituximab-containing chemotherapy protocols. The control group consisted of 9 conditionally healthy donors (mean age 52.0±7.29). Peripheral blood mononuclear cells were isolated in a Ficoll–Urografin density gradient and stained with monoclonal antibodies to identify ILC1 (CD117-CD294-), ILC2 (CD294+), ILC3 (CD117+CD294-) and NK cell subpopulations using CD3, CD16, and CD56 markers. The analysis was performed with a cytofluorimettic unit. Statistical evaluation was performed by the Mann–Whitney test (p 0.05). The obtained data showed that patients with NHL had a decreased relative number of ILC1 and ILC2 among peripheral blood mononuclear cells compared to a group of healthy donors, while the ILC3 level did not differ from the control group. An assessment of ILC distribution revealed a trend towards a decreased proportion of ILC1 in patients, while the proportions of ILC2 and ILC3 did not differ significantly. Analysis of NK cells revealed a significant increase in the ratio of CD16-CD56+ cells in patients with non-Hodgkin's lymphomas compared to donors. It was shown that patients with NHL exhibit changes in the subpopulation composition of innate lymphoid cells and NK cells. This may reflect a suppression of antitumor immunity and disturbed maturation of NK cells. The obtained data indicate a potential involvement of ILC and NK cells in pathogenesis of non-Hodgkin's lymphomas, thus requiring further research in this field.

Multiple myeloma is a malignant tumor disease that affects plasma cells and is one of the most common tumors of lymphoid origin. In the process of oncogenesis, that is, the formation of a tumor, there is a significant change in the immune balance in the body, which leads to the suppression of the immune response to the tumor. This suppression is one of the reasons why the tumor can progress and cause serious health problems for the patient. One of the key factors that affect immune balance is innate lymphoid cells (ILCs). ILCs play an important role in regulating the immune response and can both promote and hinder the development of tumor processes, depending on their functional state and interaction with other cells of the immune system. It has been shown that the number of immature CD5+ILC2s cells in the peripheral blood of patients with multiple myeloma is comparable to that of healthy individuals. However, autologous hematopoietic stem cell transplantation in MM patients leads to an increase in the relative number of CD5+ILC2s.

Background/Objectives: Multiple myeloma (MM) is characterized by complex interactions between tumor plasma cells and the tumor microenvironment, in which immune escape mechanisms play a key role. Non-classical major histocompatibility complex (MHC) molecules HLA-E and HLA-G are receptors capable of suppressing the activity of NK cells and T lymphocytes. However, their expression on immune cells in oncology, particularly in MM, remains poorly understood. Methods: Peripheral blood mononuclear cells from patients with MM and healthy controls were used as study material. HLA-E and HLA-G expression on T lymphocytes and monocytes was analyzed using flow cytometry. Results: MM was shown to be associated with increased expression of non-classical molecule HLA-E by T lymphocytes and monocytes, as well as an increased proportion of cells with phenotype HLA-E+HLA-DR+ among cells. Conclusions: Our study demonstrates that non-classical HLA-E molecule are actively expressed on immune cells in multiple myeloma, which may serve as a mechanism for tumor immune evasion. These data support further exploration of HLA-E as potential target for MM immunotherapy.

Multiple myeloma (MM) is a malignant plasma cell disorder and one of the most common tumors of lymphoid origin. In the process of oncogenesis, there is a significant change in the immune balance in the body, which leads to the suppression of the immune response to the tumor. This immune suppression is one of the reasons why the tumor can progress and cause serious health problems for the patient. One of the key factors that affect immune balance is innate lymphoid cells (ILCs). ILCs play an important role in regulating the immune response and can both promote and hinder the development of tumor processes, depending on their functional state and interaction with other cells of the immune system. Among ILCs, ILC1 mainly exert antitumour activity, but ILC2 and ILC3 are usually protumorigenic. One of the standard treatments for MM is autologous hematopoietic stem cell transplantation (auto-HSCT), and the aim of our study was to evaluate the effect of auto-HSCT on ILCs in MM. We assessed the number and subpopulation composition of ILCs in MM patients before and after auto-HSCT. In MM patients, an increase in the proportion of ILC2 and a decrease in ILC1 are observed before auto-HSCT compared to healthy controls. The subpopulation composition of ILCs changes in patients with multiple myeloma after auto-HSCT, with an increase in ILC1 and a decrease in ILC2 compared to pre-auto-HSCT values. No differences were observed in the relative number of different types of ILC in MM patients after auto-HSCT and in healthy controls. It has been shown that the number of immature CD5⁺ILC2s in the peripheral blood of patients with multiple myeloma is comparable to that of healthy individuals. However, in MM patients, HSCT leads to an increase in the relative number of CD5⁺ILC2s.