Involvement of inflammation in autoinflammation and autoimmune disease

抄録

Various recent studies reveal that many autoinflammatory syndromes result from inflammasome related protein abnormality. Some inflammasomes closely correlate with caspase 1. Caspase 1 is a key molecule for activation of IL-1β, which is responsible for induction and augmentation of inflammation. Inflammatory cytokines, including IL-1β, are necessary for T_H17 differentiation from T_H0 cell. T_H17 cells were recently reported to play major roles in autoantibody production. In this point of view, inflammasome inducing inflammation participates in prominent roles both in autoinflammatory syndromes and autoimmunity. On the other hand, non-immunological ischemic injury deeply correlates with immunological reaction in kidney transplantation. Inflammation would share significant part both in non-immunological tissue destruction and immunological reaction of rejection in kidney transplantation. Inflammatory cytokines, including IL-1β, and chemokines are key regulators in progression of inflammatory reaction in ischemic kidney injury. Our data indicate that specific chemokines or chemokine receptors participate in specific pathologic changes at specific time points in the injury. One of some molecules, which work for these pathological changes would be new therapeutic targets for transplantation.