Lupus & antiphospholipid syndrome
Platelet LGALS3BP as a Mediator of Myeloid Inflammation in Systemic Lupus Erythematosus
Main finding · Platelet LGALS3BP expression (RNA sequencing)Result — go to the resultFold change 4.0Authors' conclusion
Our results support that platelets act as potent effector cells that contribute to the pathogenesis of SLE by secreting proinflammatory LGALS3BP, which also represents a novel biomarker of SLE clinical activity.
Study context
- Population
- Patients with systemic lupus erythematosus (SLE) and age-, sex-, and race/ethnicity-matched healthy controls
- Participants
- 54 vs 18
- Comparison
- Platelets from patients with SLE vs matched healthy controls
- SLEn = 54
- Healthy controlsn = 18reference
- Outcome
- Platelet LGALS3BP expression (RNA sequencing)
Methodological detailsage-, sex-, and race/ethnicity-matched healthy controls, platelet RNA sequencing
- Age-, sex-, and race/ethnicity-matched healthy controls
- Platelet RNA sequencing
Main finding
As reported in the abstract
Fold change
4.0
adjusted P = 6.02 × 10-11
- Platelet-released LGALS3BP correlated with circulating LGALS3BP (R)
- 0.69
- Circulating LGALS3BP correlated with SLEDAI severity (r)
- 0.32
Further findings
Circulating LGALS3BP levels, LN vs inactive disease
P < 0.001
In vitro mechanistic findings
- Interferon-α induced LGALS3BP transcription and translation in MEG-01 cells in a dose-dependent manner
- Recombinant LGALS3BP and SLE platelet releasates enhanced proinflammatory cytokine production by macrophages
Original publication
Platelet LGALS3BP as a Mediator of Myeloid Inflammation in Systemic Lupus Erythematosus. Arthritis Rheumatol. Published 14 March 2023. doi:10.
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