The systemic inflammatory response is evident in inflammatory diseases, and the immune system secretes many cytokines involved, resulting in a robust immune response. For example, the pathogenesis of sepsis includes abnormal immune cell activation in the early stages as well as sepsis-related immunosuppression. During the immunosuppressive phase, CD4+ T cells, CD8+ T cells, Th17 cells, and γδ T cells are reduced while regulatory T cells increase. At the same time, T lymphocytes and neutrophils, as immune effector cells, interact with each other and play a key role in regulating the immune response to immune-inflammatory diseases. The increased release of neutrophil extracellular trap networks (NETs) by neutrophils leads to a significant upregulation of NETs-DNA-MPO, which further aggravates the septic inflammatory response and organ functional impairment. Therefore, it is important to deeply investigate the characteristic clinical immune phenotypes and molecular mechanisms associated with inflammatory diseases, and targeting therapies against them may provide new ideas for the precise treatment of diseases.
The goal of this Research Topic is to provide a forum to advance research on the contribution of the fundamental mechanisms of immune system development and function, with special emphasis on the description and mechanism of clinical immunological phenotypes in different immune disorders and the definition of their molecular basis.
The Research Topic had the bullet points including but not limited to the following:
1) Description of the immune phenotypes of various common acute and chronic diseases;
2) The regulatory mechanisms of different factors on the development and function of the host immune system;
3) Inflammatory immunological mechanisms, organ function, and interorgan interactions.
The systemic inflammatory response is evident in inflammatory diseases, and the immune system secretes many cytokines involved, resulting in a robust immune response. For example, the pathogenesis of sepsis includes abnormal immune cell activation in the early stages as well as sepsis-related immunosuppression. During the immunosuppressive phase, CD4+ T cells, CD8+ T cells, Th17 cells, and γδ T cells are reduced while regulatory T cells increase. At the same time, T lymphocytes and neutrophils, as immune effector cells, interact with each other and play a key role in regulating the immune response to immune-inflammatory diseases. The increased release of neutrophil extracellular trap networks (NETs) by neutrophils leads to a significant upregulation of NETs-DNA-MPO, which further aggravates the septic inflammatory response and organ functional impairment. Therefore, it is important to deeply investigate the characteristic clinical immune phenotypes and molecular mechanisms associated with inflammatory diseases, and targeting therapies against them may provide new ideas for the precise treatment of diseases.
The goal of this Research Topic is to provide a forum to advance research on the contribution of the fundamental mechanisms of immune system development and function, with special emphasis on the description and mechanism of clinical immunological phenotypes in different immune disorders and the definition of their molecular basis.
The Research Topic had the bullet points including but not limited to the following:
1) Description of the immune phenotypes of various common acute and chronic diseases;
2) The regulatory mechanisms of different factors on the development and function of the host immune system;
3) Inflammatory immunological mechanisms, organ function, and interorgan interactions.