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• W2802507673 abstract "The chronic inflammation associated with rheumatoid arthritis (RA) leads to focal and systemic bone erosion of the joints resulting in a crippling disability. Recent reports indicate an increase in the incidence of RA in the coming years, placing a significant burden on healthcare resources. The incidence of RA is observed to be increasing with age and a significant proportion of those new cases will be aggressively erosive.The altered physiology, due to immune disturbances, contributes towards RA pathogenesis. The imbalance of inflammatory cytokines and non-cytokine immune modulators such as prostaglandin E2 (PGE2) and IL-23-induced pathogenic IL-17, plays a crucial role in persistent inflammation and bone degradation during RA. However, the molecular mechanism of IL-23, a key cytokine, and PGE2 in the development and perpetuation of IL-17 producing effector Th17 cells is poorly understood.This review focuses on research findings that provide insight into the contribution of PGE2 and IL-23 during the development of pathogenic Th17 cells. We also highlight the key transcriptional factors required for Th17 development and therapeutic strategies to disrupt the interaction between IL-23 and IL-17 to prevent the end-organ damage in RA." @default.
• W2802507673 created "2018-05-17" @default.
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• W2802507673 date "2018-04-30" @default.
• W2802507673 modified "2023-09-26" @default.
• W2802507673 title "Prostaglandin E2 and IL-23 interconnects STAT3 and RoRγ pathways to initiate Th17 CD4+ T-cell development during rheumatoid arthritis" @default.
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• W2802507673 doi "https://doi.org/10.1007/s00011-018-1153-8" @default.
• W2802507673 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6071319" @default.
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• W2802507673 hasPublicationYear "2018" @default.
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