Lupus & antiphospholipid syndrome
Platelet TLR7 is essential for the formation of platelet–neutrophil complexes and low-density neutrophils in lupus nephritis
Authors' conclusion
LDNs sediment in the upper PBMC fraction due to PNC formation, which is dependent on the expression of TLR7 in platelets.
Study context
- Population
- SLE patients and controls; cohort of 290 SLE patients for organ damage associationSLE cohort
- Participants
- 290 patients
Methodological detailsflow cytometry, mRNA sequencing datasets and RT-PCR, platelet-HDN mixing studies in TLR7-deficient mice and Klinefelter syndrome patients
- Flow cytometry
- mRNA sequencing datasets and RT-PCR
- platelet-HDN mixing studies in TLR7-deficient mice and Klinefelter syndrome patients
Main finding
As reported in the abstract
- SLE patients with active disease have more low-density neutrophils (LDNs), heterogeneous and more immature with kidney dysfunction
- LDNs are platelet bound, in contrast to high-density neutrophils (HDNs)
- LDNs settle in the peripheral blood mononuclear cell (PBMC) layer due to increased buoyancy and neutrophil degranulation from platelet binding
- PNC formation dependent on platelet TLR7; association results in increased NETosis
- Higher neutrophil:platelet ratio associated with past and current LN flares
Original publication
Platelet TLR7 is essential for the formation of platelet–neutrophil complexes and low-density neutrophils in lupus nephritis. Rheumatology (Oxford). Published 21 June 2023. doi:10.
Composed by AI from the published abstract and checked against it. How Briefs are made →