Historically, inflammation against self was considered autoimmune, a concept that stems back to the seminal observations by Ehrlich, who described serum factors now known to be autoantibodies produced by B lineage cells that mediate 'horror autotoxicus.' The 20th century elucidation of B- and T-cell adaptive immune responses cemented the understanding of the key role of adaptive immune responses in mediating pathology against self. However, Mechnikov, who shared the Nobel Prize for the discovery of phagocytosis, highlighted the most rudimentary aspect of innate immunity. Fast forward about 100 years, and an immunogenetic understanding of innate immunity led to the categorization of innate immunopathology under the umbrella term ‘autoinflammation’ and terminology such as “horror autoinflammaticus” to highlight the schism from the classical adaptive immune understanding of autoimmunity. These concepts lead to calls for a two-tiered classification of inflammation against self, but just as innate and adaptive immunity are functionally integrated, so is immunopathology in many settings and the concept of an autoimmune to autoinflammation continuum emerged with overlaps between both.
While significant advancements have been achieved, numerous unresolved inquiries persist. For example, several disorders, such as rheumatoid arthritis, systemic lupus erythematosus, systemic juvenile idiopathic arthritis, and adult-onset Still disease, are historically designated disorders of adaptive immunity. How does innate immunity play a crucial role in them? Why are MHC-I-opathies, like psoriasis and Behçet’s disease, increasingly recognized as archetype CD8 T-cell related disorders? Do innate tissue permeability barrier dysfunction and microbial dysbiosis share mechanisms that contribute to certain skin diseases and inflammatory bowel disease? Do the emerging roles of intermediate populations of lymphocytes, including gamma delta (?d) and mucosal-associated invariant T (MAIT) cells, represent a blend of adaptive immune plasticity and innate immune rapid response, potentially determining site-specific patterns of inflammation?
We welcome submissions focusing on, but not limited to, the following topics:
1) Classification of self-reactive immune mechanisms in autoimmune diseases.
2) The role of innate immune system components in the development of autoantibodies due to citrullination in rheumatoid arthritis.
3) The contribution of neutrophils and other cell groups to the IL-23/17 axis in diseases involving MHC-I-mediated peptide presentation.
4) The contribution of innate tissue permeability barrier dysfunction and microbial dysbiosis to specific adaptive immune pathological mechanisms.
5) Effects of local immune responses on systemic pathogenesis in systemic autoimmune diseases.
6) Specific functions of cellular components in linking acquired and innate immunity in autoimmune diseases.
7) Treatment approaches for autoimmune and autoinflammatory diseases.
Historically, inflammation against self was considered autoimmune, a concept that stems back to the seminal observations by Ehrlich, who described serum factors now known to be autoantibodies produced by B lineage cells that mediate 'horror autotoxicus.' The 20th century elucidation of B- and T-cell adaptive immune responses cemented the understanding of the key role of adaptive immune responses in mediating pathology against self. However, Mechnikov, who shared the Nobel Prize for the discovery of phagocytosis, highlighted the most rudimentary aspect of innate immunity. Fast forward about 100 years, and an immunogenetic understanding of innate immunity led to the categorization of innate immunopathology under the umbrella term ‘autoinflammation’ and terminology such as “horror autoinflammaticus” to highlight the schism from the classical adaptive immune understanding of autoimmunity. These concepts lead to calls for a two-tiered classification of inflammation against self, but just as innate and adaptive immunity are functionally integrated, so is immunopathology in many settings and the concept of an autoimmune to autoinflammation continuum emerged with overlaps between both.
While significant advancements have been achieved, numerous unresolved inquiries persist. For example, several disorders, such as rheumatoid arthritis, systemic lupus erythematosus, systemic juvenile idiopathic arthritis, and adult-onset Still disease, are historically designated disorders of adaptive immunity. How does innate immunity play a crucial role in them? Why are MHC-I-opathies, like psoriasis and Behçet’s disease, increasingly recognized as archetype CD8 T-cell related disorders? Do innate tissue permeability barrier dysfunction and microbial dysbiosis share mechanisms that contribute to certain skin diseases and inflammatory bowel disease? Do the emerging roles of intermediate populations of lymphocytes, including gamma delta (?d) and mucosal-associated invariant T (MAIT) cells, represent a blend of adaptive immune plasticity and innate immune rapid response, potentially determining site-specific patterns of inflammation?
We welcome submissions focusing on, but not limited to, the following topics:
1) Classification of self-reactive immune mechanisms in autoimmune diseases.
2) The role of innate immune system components in the development of autoantibodies due to citrullination in rheumatoid arthritis.
3) The contribution of neutrophils and other cell groups to the IL-23/17 axis in diseases involving MHC-I-mediated peptide presentation.
4) The contribution of innate tissue permeability barrier dysfunction and microbial dysbiosis to specific adaptive immune pathological mechanisms.
5) Effects of local immune responses on systemic pathogenesis in systemic autoimmune diseases.
6) Specific functions of cellular components in linking acquired and innate immunity in autoimmune diseases.
7) Treatment approaches for autoimmune and autoinflammatory diseases.