About this Research Topic
Autoimmune diseases represent a clinically significant segment of medicine. Indeed, mechanisms for auto-antibody formation, new disease biomarkers and predictors of clinical outcomes are currently at the forefront of scientific research. Auto-inflammatory conditions are less frequent but are often associated with severe clinical cases which require rapid recognition and interpretation.
Furthermore, genetic features of auto-inflammatory diseases represent a rapidly evolving issue in research that has already undergone a significant evolution over the last few years. In addition, new mediators of inflammation have been discovered in rapid sequence and mechanisms of inflammatory lesions have recently been explained on a genetic basis. In this respect, therapeutic evolution has been impressive and clinical results are highly relevant.
The kidney is a target organ in almost all auto-immune diseases and is also frequently involved in auto-inflammatory processes. In light of this backdrop, this Research Topic on the kidney in auto-immune and auto-inflammatory diseases is dedicated to tracing the most recent research that links the pathological conditions with renal lesions. We are particularly interested in new evidence on mechanisms that induce the formation of amyloid and how amyloid is linked with the glomerular degeneration. Amyloidosis is a well-characterized malignant condition that may lead to the accumulation of amyloid in glomeruli.
Systemic Lupus Erythematosus and generally interferonopathies are also areas of interest in this Research Topic. Lupus nephritis is the main example of selective organ autoimmune pathology occurring in a systemic disorder (SLE), while deposition of antibodies formed in circulation is the major pathogenetic mechanism. The characterization of new glomerular antigens specific for Lupus nephritis pathology classes and of new antibodies is a key passage for any evolution. The characterization of ‘nephritogenic antibodies’ also has a role in identifying new mechanisms of formation and in suggesting novel targeted therapeutic approaches. Furthermore, a section would be dedicated to explaining the link between the formation of ‘nephritogenic auto-antibodies’ and new concepts on the pathogenesis of SLE. More specifically, we plan to discuss how DNase defects and γ-interferon may impact auto-antibodies generation.
Moreover, we would like to gather manuscripts around the broad field of inflammatory diseases affecting small and large vessels, which would start with the presentation of new concepts on conditions that have an early onset - such as STING-associated vasculopathy with onset in infancy (SAVI) - and then continue by focussing on classical aspects of small vessel vasculitis including Genetics, the role of Complement and with a specific focus on Eosinophilic granulomatosis with polyangiitis and aortitis.
We welcome the submission of Review and Original Research articles, Opinion and Perspective covering, but not limited to, the following aspects:
1) Auto-inflammatory diseases: amyloidosis and beyond
• Classification, genetic bases and clinical presentation of Autoinflammatory diseases
• Renal manifestations of AA amyloidosis
• The role of NLRP3 inflammasome in acute and chronic kidney diseases
• PAPA syndrome: two cases report
2) Type 1 Interferonopathies
• Classification of Type 1 Interferonopathies. A survey on associated renal injury
• Extra-nucleic acids, is it all a matter of localization?
• Mendelian diseases linked to defective DNase activity: DNase1L3, DNase2, DNase3, TREX1.
3)Lupus nephritis: behind DNA
• The spectrum of auto-antibodies against podocyte antigens and specific isotypes in Lupus Nephritis.
• New class-specific antigens for Lupus nephritis.
• Podocyte antigens for autoimmunity in Lupus nephritis: NETosis is a post-translational modifier of their structure
• NETs degradation and Lupus nephritis
• NETs and mitochondrial DNA contribute to lupus-like disease in mice
• NET equivalents or mimics
• Adaptive immunity versus NETs components.
• Modulation of NETosis by drugs ‘in vitro’.
4)Inflammatory diseases affecting small and large vessels
• Vasculopathy in autoinflammatory diseases (SAVI, ADA2 deficiency, etc.)
• Genetics of small vessel vasculitis
• Renal histopathology of small vessel vasculitis.
• The complement system in renal vasculitis and glomerulonephritis: pathogenic role and therapeutic inhibition
• Eosinophilic granulomatosis with polyangiitis (Churg-Strauss syndrome)
• Aortitis and periaortitis
Furthermore, genetic features of auto-inflammatory diseases represent a rapidly evolving issue in research that has already undergone a significant evolution over the last few years. In addition, new mediators of inflammation have been discovered in rapid sequence and mechanisms of inflammatory lesions have recently been explained on a genetic basis. In this respect, therapeutic evolution has been impressive and clinical results are highly relevant.
The kidney is a target organ in almost all auto-immune diseases and is also frequently involved in auto-inflammatory processes. In light of this backdrop, this Research Topic on the kidney in auto-immune and auto-inflammatory diseases is dedicated to tracing the most recent research that links the pathological conditions with renal lesions. We are particularly interested in new evidence on mechanisms that induce the formation of amyloid and how amyloid is linked with the glomerular degeneration. Amyloidosis is a well-characterized malignant condition that may lead to the accumulation of amyloid in glomeruli.
Systemic Lupus Erythematosus and generally interferonopathies are also areas of interest in this Research Topic. Lupus nephritis is the main example of selective organ autoimmune pathology occurring in a systemic disorder (SLE), while deposition of antibodies formed in circulation is the major pathogenetic mechanism. The characterization of new glomerular antigens specific for Lupus nephritis pathology classes and of new antibodies is a key passage for any evolution. The characterization of ‘nephritogenic antibodies’ also has a role in identifying new mechanisms of formation and in suggesting novel targeted therapeutic approaches. Furthermore, a section would be dedicated to explaining the link between the formation of ‘nephritogenic auto-antibodies’ and new concepts on the pathogenesis of SLE. More specifically, we plan to discuss how DNase defects and γ-interferon may impact auto-antibodies generation.
Moreover, we would like to gather manuscripts around the broad field of inflammatory diseases affecting small and large vessels, which would start with the presentation of new concepts on conditions that have an early onset - such as STING-associated vasculopathy with onset in infancy (SAVI) - and then continue by focussing on classical aspects of small vessel vasculitis including Genetics, the role of Complement and with a specific focus on Eosinophilic granulomatosis with polyangiitis and aortitis.
We welcome the submission of Review and Original Research articles, Opinion and Perspective covering, but not limited to, the following aspects:
1) Auto-inflammatory diseases: amyloidosis and beyond
• Classification, genetic bases and clinical presentation of Autoinflammatory diseases
• Renal manifestations of AA amyloidosis
• The role of NLRP3 inflammasome in acute and chronic kidney diseases
• PAPA syndrome: two cases report
2) Type 1 Interferonopathies
• Classification of Type 1 Interferonopathies. A survey on associated renal injury
• Extra-nucleic acids, is it all a matter of localization?
• Mendelian diseases linked to defective DNase activity: DNase1L3, DNase2, DNase3, TREX1.
3)Lupus nephritis: behind DNA
• The spectrum of auto-antibodies against podocyte antigens and specific isotypes in Lupus Nephritis.
• New class-specific antigens for Lupus nephritis.
• Podocyte antigens for autoimmunity in Lupus nephritis: NETosis is a post-translational modifier of their structure
• NETs degradation and Lupus nephritis
• NETs and mitochondrial DNA contribute to lupus-like disease in mice
• NET equivalents or mimics
• Adaptive immunity versus NETs components.
• Modulation of NETosis by drugs ‘in vitro’.
4)Inflammatory diseases affecting small and large vessels
• Vasculopathy in autoinflammatory diseases (SAVI, ADA2 deficiency, etc.)
• Genetics of small vessel vasculitis
• Renal histopathology of small vessel vasculitis.
• The complement system in renal vasculitis and glomerulonephritis: pathogenic role and therapeutic inhibition
• Eosinophilic granulomatosis with polyangiitis (Churg-Strauss syndrome)
• Aortitis and periaortitis
Keywords: Amyloidosis, Systemic Lupus Erythematosus, Lupus nephritis, PAPA syndrome, DNAse2 and 1L3, interferonopathies, NETosis, SAVI, Small Vessel Vasculitis, Eosinophilic granulomatosis with polyangiitis, aortitis
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