Emerging role of leptin in joint inflammation and destruction.
Haruka TsuchiyaKeishi FujioPublished in: Immunological medicine (2021)
Rheumatoid arthritis (RA) is an autoimmune disease characterized by tumor-like hyperplasia and inflammation of the synovium, which causes synovial cell invasion into the bone and cartilage. In RA pathogenesis, various molecules in effector cells (i.e., immune cells and mesenchymal cells) are dysregulated by genetic and environmental factors. Consistent with the early stages of RA, these pathogenic cells cooperate and activate each other directly by cell-to-cell contact or indirectly via humoral factors. Recently, growing evidence has revealed essential role of adipokines, which are multifunctional signal transduction molecules, in the immune system. In this review, we summarize the current understanding of the cross-talk between leptin, one of the most well-known and best-characterized adipokines, and osteoimmunology. Furthermore, we discuss the contribution of leptin to the pathogenesis of RA and its potential mechanisms.
Keyphrases
- rheumatoid arthritis
- induced apoptosis
- cell cycle arrest
- disease activity
- single cell
- oxidative stress
- stem cells
- systemic lupus erythematosus
- endoplasmic reticulum stress
- interstitial lung disease
- multiple sclerosis
- cancer therapy
- cell death
- body composition
- regulatory t cells
- pi k akt
- systemic sclerosis
- mesenchymal stem cells
- extracellular matrix
- postmenopausal women
- idiopathic pulmonary fibrosis