Prostaglandin E2 and IL-23 interconnects STAT3 and RoRγ pathways to initiate Th17 CD4+ T-cell development during rheumatoid arthritis
Autor: | Aleksandra Ignatowicz, Keya Meyers, Rangaiah Shashidharamurthy, William G Cumbie, Lauren Holland, Anna McClain, Janaiya Samuels, Daryllynn Nelson, María Graciela López |
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Rok vydání: | 2018 |
Předmět: |
030203 arthritis & rheumatology
0301 basic medicine Pharmacology biology business.industry medicine.medical_treatment Immunology Inflammation medicine.disease Proinflammatory cytokine 03 medical and health sciences 030104 developmental biology 0302 clinical medicine Immune system Cytokine RANKL Rheumatoid arthritis medicine biology.protein Interleukin 23 Interleukin 17 medicine.symptom business |
Zdroj: | Inflammation Research. 67:589-596 |
ISSN: | 1420-908X 1023-3830 |
Popis: | 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. |
Databáze: | OpenAIRE |
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