Interaction of NLRP3-Inflammasoma with autoimmune diseases: a literature review
DOI:
https://doi.org/10.18227/hd.v4i1.7519Keywords:
Inflammasome, autoimmune diseases, rheumatoid arthritis, type I diabetes mellitus, systemic lúpus erythematosus, multiple sclerosisAbstract
Introduction: Among the protection mechanisms of the immune system, there is the protein-inflammasome complex. This intracellular complex acts as a sensor and mediator of danger signals, being formed by three basic structures: NOD-type receptor, ASC adapter protein and pro-caspase1. Once activated, it is able to induce interleukin maturation and secretion, mainly IL-1β and IL-18. However, the deregulation of this molecular platform has been associated with the development and progression of many inflammatory and autoimmune diseases. Methods: Bibliographic review using the academic Google, Medline, as databases. Center for Biotechnology Information (PubMed) and the Scientific Electronic Electronic Library Online (SciELO) electronic library. The search was carried out in articles published from 2000 to 2020, in Portuguese and /or English, with the keywords inflammasome, autoimmune disease, rheumatoid arthritis, type I diabetes mellitus, systemic lupus erythematosus and multiple sclerosis. Development: An etiological relationship between autoimmune diseases and inflammasome activation has been shown. Studies have demonstrated the importance of the protein complex in the regulation of innate immunity and its significance in autoimmune diseases. Conclusion: This analysis demonstrated that the loss of self-tolerance involved in autoimmune diseases is substantially related to the exacerbated production of cytokines IL-1β and IL-18 due to the altered genes resulting from the activation of the NLR-Inflamasome complex.
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