Leukocyte Ig-like receptor A3 facilitates inflammation, migration and invasion of synovial tissue-derived fibroblasts via ERK/JNK activation
Authors' conclusion
The present study provides the first evidence that soluble LILRA3 is a novel proinflammatory mediator involved in synovial inflammation by promoting RA-FLS activation, migration and invasion, probably through the ERK/JNK signalling pathways.
Study context
- Population
- Patients with RA; RA-FLSs
- Outcome
- Pathological role of LILRA3 in RA joint inflammation
Methodological detailsin vitro
- In vitro
Main finding
As reported in the abstract
- Soluble Leukocyte Ig-like receptor A3 (LILRA3) specifically expressed in synovial fluid; serum LILRA3 significantly increased and positively correlated with disease activity/severity in RA
- LILRA3 induced increased IL-6, IL-8 and MMP3 expression in RA-FLSs
- LILRA3 stimulation or overexpression promoted RA-FLS migration and invasion and enhanced ERK/JNK phosphorylation
- ERK/JNK inhibition suppressed IL-6/IL-8 expression in LILRA3-stimulated RA-FLSs
- LILRA3 co-localized with LILRB1 and HLA-G in RA-FLSs
Original publication
Leukocyte Ig-like receptor A3 facilitates inflammation, migration and invasion of synovial tissue-derived fibroblasts via ERK/JNK activation. Rheumatology (Oxford). Published 18 July 2023. doi:10.
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