About this Research Topic
This Research Topic is the second volume of the “Pathogenetic Mechanism and therapeutic target for Inflammation in autoimmune disease”. Please see the first volume here
Inflammation is a defensive response of the body to external stimuli such as pathogenic microorganisms. However, the inflammatory response continues in several chronic illnesses and results in significant tissue and organ damage. In recent years, accumulating pieces of evidence have suggested that the abnormal inflammatory response is involved in many chronic diseases, especially in autoimmune diseases (ADs), such as inflammatory bowel disease, rheumatoid arthritis, and systemic lupus erythematosus. Although the pro-inflammatory cytokines and mediators that trigger ADs have been the focus of intense investigations, the exact role of inflammation dysfunction in ADs is still unclear. Treatment of these illnesses will greatly benefit from a better understanding of how inflammation is controlled in ADs.
It has been revealed that Th1 and Th17 cells are important cellular mediators of inflammation in ADs. The specific cytokine environment in the site of inflammation or secondary lymphatic tissues is important in the initiation and effect phase phases of T cell response. Regulatory B cells suppress inflammation by inhibiting the differentiation of Th1 and Th17 immune responses in the development of ADs. Inflammation is regulated and resolved in ADs by cytokine-mediated processes including Th2 activation induced by IL-4 and IL-13, the elimination of inflammation by IL-9, eosinophil expansion induced by IL-5, macrophage polarization mediated by IL-33, the IL-10 production by regulatory B cells and the suppression of lymphoid follicle formation mediated by IL-27. Recent research has shown that systemic inflammation is essential for the correct control of the organismal level. Therefore, it is crucial to further elucidate the pathogenetic mechanism and therapeutic target for inflammation in ADs.
The goal of this Research Topic is to provide a forum to advance research on the contribution of understanding the mechanism of inflammation regulation in ADs. Moreover, we will also explore ways to control the suppression and regression of inflammation in ADs, ultimately achieving beneficial effects on ADs by identifying specific new targets.
We welcome the submission of Original Research and Review articles, including but not limited to the following:
- Organ or tissue inflammation in ADs
- Emerging inflammatory biomarkers for ADs
- The exploration of inflammatory signaling pathways in ADs
- Pathogenetic mechanism of inflammation in ADs
- Identifying novel therapeutic target for inflammation in ADs
- Discovery of new anti-inflammatory therapies for ADs
Inflammation is a defensive response of the body to external stimuli such as pathogenic microorganisms. However, the inflammatory response continues in several chronic illnesses and results in significant tissue and organ damage. In recent years, accumulating pieces of evidence have suggested that the abnormal inflammatory response is involved in many chronic diseases, especially in autoimmune diseases (ADs), such as inflammatory bowel disease, rheumatoid arthritis, and systemic lupus erythematosus. Although the pro-inflammatory cytokines and mediators that trigger ADs have been the focus of intense investigations, the exact role of inflammation dysfunction in ADs is still unclear. Treatment of these illnesses will greatly benefit from a better understanding of how inflammation is controlled in ADs.
It has been revealed that Th1 and Th17 cells are important cellular mediators of inflammation in ADs. The specific cytokine environment in the site of inflammation or secondary lymphatic tissues is important in the initiation and effect phase phases of T cell response. Regulatory B cells suppress inflammation by inhibiting the differentiation of Th1 and Th17 immune responses in the development of ADs. Inflammation is regulated and resolved in ADs by cytokine-mediated processes including Th2 activation induced by IL-4 and IL-13, the elimination of inflammation by IL-9, eosinophil expansion induced by IL-5, macrophage polarization mediated by IL-33, the IL-10 production by regulatory B cells and the suppression of lymphoid follicle formation mediated by IL-27. Recent research has shown that systemic inflammation is essential for the correct control of the organismal level. Therefore, it is crucial to further elucidate the pathogenetic mechanism and therapeutic target for inflammation in ADs.
The goal of this Research Topic is to provide a forum to advance research on the contribution of understanding the mechanism of inflammation regulation in ADs. Moreover, we will also explore ways to control the suppression and regression of inflammation in ADs, ultimately achieving beneficial effects on ADs by identifying specific new targets.
We welcome the submission of Original Research and Review articles, including but not limited to the following:
- Organ or tissue inflammation in ADs
- Emerging inflammatory biomarkers for ADs
- The exploration of inflammatory signaling pathways in ADs
- Pathogenetic mechanism of inflammation in ADs
- Identifying novel therapeutic target for inflammation in ADs
- Discovery of new anti-inflammatory therapies for ADs
Keywords: autoimmune disease, inflammation, chronic diseases, pathogenetic mechanism
Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.
