Inflammasomes in Sjögren’s Disease: Exploring the Therapeutic Value

Inflammasomes arise from complex protein assembly mechanisms and play a fundamental role in managing inflammation and the innate immune response. The molecules that trigger inflammasome assembly and activation are molecules derived from pathogens or DNA fragments released following cellular damage. The phenomena resulting from inflammasome activation range from the activation of caspases, such as caspase-1, to the secretion of pro-inflammatory cytokines, to cellular death by apoptosis or pyroptosis. Various diseases have been linked to aberrant inflammasome activation, including several autoimmune diseases, leading scientists to direct experiments toward identifying the mechanisms responsible for aberrant inflammasome activation so as to develop new therapeutic strategies. In this review, we summarize the assembly mechanisms and involvement of two specific inflammasomes, NLRP3 and AIM2, in autoimmune Sjögren’s disease (SjD). NLRP3 and AIM2 aberrant activations appear to be involved in the exacerbation of inflammation, which becomes chronic, leading to dry mouth and dry eye and to an increased risk of developing B-cell non-Hodgkin’s lymphoma in these patients. Understanding how different inflammasomes contribute to the pathogenesis of SjD could be fundamental to a better understanding of the complex molecular mechanisms underlying this disease.