Regulatory role of KCa3.1 in immune cell function and its emerging association with rheumatoid arthritis

Rheumatoid arthritis (RA) is a common autoimmune disease characterized by chronic inflammation. Immune dysfunction is an essential mechanism in the pathogenesis of RA and directly linked to synovial inflammation and cartilage/bone destruction. Intermediate conductance Ca 2+ -activated K + channel (K...

Full description

Saved in:
Bibliographic Details
Published in:Frontiers in immunology 2022-10, Vol.13, p.997621-997621
Main Authors: Lin, Yi, Zhao, Ying-Jie, Zhang, Hai-Lin, Hao, Wen-Juan, Zhu, Ren-Di, Wang, Yan, Hu, Wei, Zhou, Ren-Peng
Format: Article
Language:English
Subjects:
immune cells
Immunology
joint inflammation
KCa3.1
rheumatoid arthritis
synovitis
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Rheumatoid arthritis (RA) is a common autoimmune disease characterized by chronic inflammation. Immune dysfunction is an essential mechanism in the pathogenesis of RA and directly linked to synovial inflammation and cartilage/bone destruction. Intermediate conductance Ca 2+ -activated K + channel (KCa3.1) is considered a significant regulator of proliferation, differentiation, and migration of immune cells by mediating Ca 2+ signal transduction. Earlier studies have demonstrated abnormal activation of KCa3.1 in the peripheral blood and articular synovium of RA patients. Moreover, knockout of KCa3.1 reduced the severity of synovial inflammation and cartilage damage to a significant extent in a mouse collagen antibody-induced arthritis (CAIA) model. Accumulating evidence implicates KCa3.1 as a potential therapeutic target for RA. Here, we provide an overview of the KCa3.1 channel and its pharmacological properties, discuss the significance of KCa3.1 in immune cells and feasibility as a drug target for modulating the immune balance, and highlight its emerging role in pathological progression of RA.
ISSN:1664-3224
1664-3224
DOI:10.3389/fimmu.2022.997621