Department of Microbiology and Immunology, University of North Carolina at Chapel Hill, Chapel Hill, NC, United States.
Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, NC, United States.
Front Immunol. 2023 Apr 4;14:1154552. doi: 10.3389/fimmu.2023.1154552. eCollection 2023.
Inflammasome molecules make up a family of receptors that typically function to initiate a proinflammatory response upon infection by microbial pathogens. Dysregulation of inflammasome activity has been linked to unwanted chronic inflammation, which has also been implicated in certain autoimmune diseases such as multiple sclerosis, rheumatoid arthritis, type 1 diabetes, systemic lupus erythematosus, and related animal models. Classical inflammasome activation-dependent events have intrinsic and extrinsic effects on both innate and adaptive immune effectors, as well as resident cells in the target tissue, which all can contribute to an autoimmune response. Recently, inflammasome molecules have also been found to regulate the differentiation and function of immune effector cells independent of classical inflammasome-activated inflammation. These alternative functions for inflammasome molecules shape the nature of the adaptive immune response, that in turn can either promote or suppress the progression of autoimmunity. In this review we will summarize the roles of inflammasome molecules in regulating self-tolerance and the development of autoimmunity.
炎症小体分子构成了一组受体家族,这些受体通常在受到微生物病原体感染时发挥启动促炎反应的作用。炎症小体活性的失调与不受欢迎的慢性炎症有关,而慢性炎症也与某些自身免疫性疾病有关,如多发性硬化症、类风湿性关节炎、1 型糖尿病、系统性红斑狼疮和相关的动物模型。经典的炎症小体激活依赖性事件对固有和适应性免疫效应器以及靶组织中的固有细胞都有内在和外在的影响,这些都可能导致自身免疫反应。最近,炎症小体分子也被发现可以独立于经典炎症小体激活的炎症来调节免疫效应细胞的分化和功能。这些炎症小体分子的替代功能塑造了适应性免疫反应的性质,而适应性免疫反应反过来又可以促进或抑制自身免疫的进展。在这篇综述中,我们将总结炎症小体分子在调节自身耐受和自身免疫发生中的作用。