About this Research Topic
IgA nephropathy (IgAN) is the most common primary glomerulonephritis in the world, and because of its poor prognosis, there are still many patients worldwide who suffer from chronic renal failure due to this disease and undergo renal replacement therapy. In recent years, however, the pathogenesis of the disease has been elucidated and surrogate endpoints for treatment have been established, leading to rapid progress in the development of new drugs.
The development of new drugs has been driven by the evidence that immune complexes composed of galactose-deficient IgA1 (GdIgA1), an aberrant O-glycosylation of the IgA1 hinge region, and autoantibodies that recognize it are the key inflammatory molecules in the pathogenesis of this disease, and the finding that the primary responsible B cells are mucosa-derived plasma cells.
However, there remain many unresolved pathogenesis and pathophysiology. In this Research Topic, we want to encourage authors to submit their research on any of the following subtopics:
1. Mucosal immune dysregulation and GdIgA1 production
2. Nasopharyngeal associated mucosa and IgA nephropathy
3. Gut associated mucosa and IgA nephropathy
4. Autoimmune diseases and mucosal bacterial flora
5. IgA nephropathy (IgAN) and mucosal flora
6. Mucosal immune abnormalities and genetic background in IgAN
7. Autoimmune properties of IgAN
8. B-cell abnormalities in IgAN, including homing abnormalities
9. Role of APRIL in IgAN Pathogenesis
10. Role of BAFF in IgAN Pathogenesis
11. Role of TLR in IgAN Pathogenesis
We hope that each expert from various fields will summarize and discuss these unresolved issues based on the latest findings, thereby helping to elucidate the pathogenesis of the disease and to implement new drugs.
The development of new drugs has been driven by the evidence that immune complexes composed of galactose-deficient IgA1 (GdIgA1), an aberrant O-glycosylation of the IgA1 hinge region, and autoantibodies that recognize it are the key inflammatory molecules in the pathogenesis of this disease, and the finding that the primary responsible B cells are mucosa-derived plasma cells.
However, there remain many unresolved pathogenesis and pathophysiology. In this Research Topic, we want to encourage authors to submit their research on any of the following subtopics:
1. Mucosal immune dysregulation and GdIgA1 production
2. Nasopharyngeal associated mucosa and IgA nephropathy
3. Gut associated mucosa and IgA nephropathy
4. Autoimmune diseases and mucosal bacterial flora
5. IgA nephropathy (IgAN) and mucosal flora
6. Mucosal immune abnormalities and genetic background in IgAN
7. Autoimmune properties of IgAN
8. B-cell abnormalities in IgAN, including homing abnormalities
9. Role of APRIL in IgAN Pathogenesis
10. Role of BAFF in IgAN Pathogenesis
11. Role of TLR in IgAN Pathogenesis
We hope that each expert from various fields will summarize and discuss these unresolved issues based on the latest findings, thereby helping to elucidate the pathogenesis of the disease and to implement new drugs.
Keywords: Mucosal Immune Dysregulation, IgAN, pathogenesis, IgA nephropathy
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