Lupus Nephritis Clinical Trial
Official title:
Detection of Annexin A2 in Systemic Lupus Erythematosus
There is substantial clinical and biological intra and inter-patient variability in SLE.
Vascular, renal and neurologic deficiency can be organ-threatening or even life-threatening,
leading to increased morbidity and mortality.
Thus, biomarkers of disease activity and prognosis are required for regular follow-up of SLE
patients.
Implication of Toll-like Receptors (TLRs) in SLE has been extensively studied in mice models
and humans. Self nuclear antigens bind to TLRs which are located on the surface of dendritic
cells, B-cells, and endothelial cells, leading to production of pro-inflammatory cytokines
and pathologic autoantibodies involved in organ dysfunction of SLE patients. Moreover, TLR
expression in SLE is significantly higher and significantly correlated with disease activity.
Annexin A2 (ANXA2) is a member of the annexins superfamily which exists as a monomer or
heterotetramer and is implicated in several biological processes. Most notably, it binds to
ẞ2GP1/anti-ẞ2GP1 antibodies and mediates endothelial cell activation via a TLR4 signaling
pathway, highlighting its key role in Antiphospholipid Syndrome (APS) frequently associated
with SLE.
ANXA2 is also involved in the physiopathology of SLE. Anti-DNA autoantibodies can bind with
ANXA2 expressed on mesangial cells in lupus nephritis. Besides, a french study carried out in
Amiens' University Hospital showed that vascular lesions in lupus nephritis were associated
with a significant increase in vascular expression of ANXA2.
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