Simultaneous Assessment of mTORC1, JAK/STAT, and NLRP3 Inflammasome Activation Pathways in Patients with Sarcoidosis

The unknown etiology of sarcoidosis, along with the variability in organ involvement and disease course, complicates effective treatment this disease. Based on recent studies, cellular inflammatory pathways involved granuloma formation are interest regarding possible new options, such as mechanistic (formerly mammalian) target rapamycin complex 1 (mTORC1) pathway, Janus kinase/signal transducers activators transcription (JAK/STAT) nucleotide-binding domain, leucine-rich-containing family, pyrin domain-containing-3 (NLRP3) inflammasome pathway. aim study was to explore potential coexpression these three patients sarcoidosis see whether differences were related outcome. tissue 60 used determine activity signaling using immunohistochemistry. activation NLRP3 present 85% all patients, mTORC1 JAK/STAT 49% 50% respectively. Furthermore, presence at diagnosis associated a chronic course sarcoidosis. Our finding different conceptual phenotypes could possibly guide future studies available inhibitors either NLRP3, JAK-STAT, more personalized medicine approach.