Role of the Neonatal Fc Receptor for IgG in the Pathophysiology of Lupus
Role of the Neonatal Fc Receptor for IgG in the Pathophysiology of Lupus
This study evaluates the expression of the neonatal fc receptor (FcRn) in white blood cells and antigen-presenting cells (APC) in active lupus patients compared to inactive lupus patients and control to investigate if it's upregulated or not.
FcRn is an intracellular receptor which binds the Fc of immunoglobulins G (IgG) and albumin which induce an upgraded half-life of this two proteins.
It's extended role involve the regulation of immune complexes and anti-tumoral immunity, some studies showing a direct correlation between it's expression and the tumor surface and prognosis.
Recently a role in the upregulation of humoral response with a increase of the antibodies's diversity and a more efficient priming of lymphocyte B have been evocated.
The lupus erythematosus is an auto-immune disease mediated by IgG and immune complexes characterized by a high diversity of autoantibodies and a large dysregulation of the immune system in all it's components.
In this study, by analogy with the founding in anti-tumoral immunity, the investigators hypothesised that in an active lupus disease the expression of FcRn is upregulated in the white blood cells and in APC.
This is followed by an extended half life of IgG autoantibodies and immune complexes inducing direct damages by their deposit in tissues and indirectly by upregulating the humoral response, leading to anormal production of a large panel of autoantibodies.
Inclusion criteria:
Exclusion criteria: