IgA autoantibodies promote inflammation, Th17 polarization and fibrotic responses in hidradenitis suppurativa - PubMed
5 hours ago
- #hidradenitis suppurativa
- #immune dysregulation
- #IgA autoantibodies
- IgA autoantibodies are elevated in hidradenitis suppurativa (HS) lesions and correlate with disease severity.
- IgA autoantibodies target diverse autoantigens, including nuclear, cytoplasmic, and membrane antigens.
- IgA binding to CD68+ macrophages induces TNF, IL-6, IL-1β secretion and upregulates inflammasome and profibrotic pathways.
- Anti-neutrophil extracellular trap (NET) IgA promotes NET formation, creating a pathogenic feedback loop.
- NET-IgA immune complexes drive CCL18 secretion by macrophages, leading to collagen production by fibroblasts and a type I interferon signature.
- IgA immune complexes presented by dendritic cells activate CD4+ T cells, increasing IFN-γ production and inflammation.
- Macrophages exposed to IgA polarize naïve CD4+ T cells toward a Th17 phenotype, linking innate and adaptive immune responses.
- Fibroblasts exposed to NET-IgA complexes express adhesion molecules, chemokines, and regulators of adaptive immunity.
- IgA autoantibodies are central drivers of chronic inflammation, fibrosis, and immune crosstalk in HS.