Myelodysplastic syndrome (MDS) is a complex blood disorder that involves abnormalities in the bone marrow microenvironment. The bone marrow microenvironment refers to the components of non-hematopoietic cells in the bone marrow that provide necessary support and regulation for the growth, differentiation, survival, and function of hematopoietic cells. In recent years, more and more studies have focused on the abnormalities of the bone marrow microenvironment in MDS patients, and these changes have an important impact on the occurrence, progression and prognosis of the disease.
First, there are abnormalities in the non-hematopoietic components of the bone marrow in patients with MDS. These changes may be triggered by abnormal MDS cells, but in some cases they can also be a problem with the bone marrow matrix itself. Abnormal stromal function may result in a significant effect on the hematopoietic process, even if MDS cells occupy only a small fraction of the bone marrow. This stromal abnormality may involve alterations in a variety of cytokines and other regulators. For example, increases in tumor necrosis factor and vascular endothelial growth factor have been observed in patients with MDS. These cytokines may play a role in the development of MDS by influencing the survival, proliferation, and differentiation of hematopoietic cells, as well as regulating the composition and function of the bone marrow microenvironment.
Secondly, the adaptive immune response of MDS patients is also the focus of research. Accumulating evidence suggests that immune response may play a role in the characteristics of MDS. Immunosuppression** is effective in a subset of patients with MDS, which further supports the importance of immune response in the disease. In MDS patients, a population of oligoclonal T cells with presumed autoreactivity can be observed. These T cells may play a key role in the initiation and progression of the disease. Interestingly, these T cell populations became more polyclonal after **, suggesting that the immune response may play a role in the course of the disease.
In addition, basic research has also revealed the importance of bone marrow stromal abnormalities in MDS. For example, studies in mice have shown that stromal abnormalities may contribute to hematopoietic dysfunction and inefficiency, even if hematopoietic cells are normal. In addition, the experimental results of transgenic matrix leading to the development of cloned malignant myeloid cells further underscore the critical role of matrix in MDS. Other studies have also found genetic abnormalities in stromal cells in a small number of patients with MDS. These findings provide a new perspective on the pathogenesis of MDS and highlight the importance of matrix abnormalities in it.
Finally, a subset of patients with MDS develop myelofibrosis, a late event that severely limits hematopoiesis. Although myelofibrosis is considered a late event of MDS and is unlikely to contribute to the pathogenesis of the disease, it certainly increases morbidity and mortality associated with the progression of MDS. In addition, some environmental factors such as radiotherapy and chemotherapy are also thought to be risk factors for MDS. These factors may lead to the development or progression of MDS through damage to the bone marrow, interstitium, and hematopoietic cells. However, there are still many unknowns about the specific effects of these environmental factors on the bone marrow microenvironment and how they interact with the pathogenesis of MDS.
In summary, abnormalities in the bone marrow microenvironment play a key role in the occurrence, progression, and prognosis of MDS. From cytokines to immune responses to stromal abnormalities and myelofibrosis, the study of the bone marrow microenvironment provides important clues to the understanding of the pathogenesis of MDS. Future research needs to further explore the role of these factors in MDS and their interrelationships in order to develop more effective strategies.