Nature Immunology: a new discovery against autoimmune diseases

Recently, researchers from Cincinnati Children's Hospital Medical Center and other scientific research institutions published an article entitled "T cells instruct myeloid cells to produce inflammatory-independent IL-1 β and cause autoimmunity" on Nature Immunology A new trigger T cell was found in mice to drive inflammation and cause multiple autoimmunity The molecular process of sexual diseases provides a theoretical basis for the treatment of multiple sclerosis, type 1 diabetes and inflammatory bowel disease Interleukin-1 β (IL-1 β) is the key factor of anti-bacterial immunity and autoimmune inflammation The production of IL-1 β requires innate immune receptor signal transduction and mature shear of inflammatory bodies It is not clear whether this mechanism is applicable to the production of IL-1 β in T cell driven autoimmune diseases The researchers found that IL-1 β produced an inflammatory body independent pathway, which was triggered by the homologous interaction between CD4 + T cells and mononuclear phagocytes (MPS) TNF (tumor necrosis factor) produced by activated CD4 + T cells binds to TNF receptor (TNFR) on MP, resulting in the synthesis of IL-1 β precursor The apoptotic signal transduction receptor Fas in MP is activated by Fas ligand (FasL) expressed by CD4 + T cells, resulting in caspase-8 dependent IL-1 β precursor shear Mature IL-1 β leads to systemic inflammation, while the absence of TNFR or Fas signal can protect mice from CD4 + T cell driven autoimmunity The TNFR – Fas – caspase-8 dependent pathway provides a mechanism for IL-1 β production and its role in CD4 + T cell driven autoimmune pathology