The role of FcRn in autoimmune diseases remains to be clarified, but it has been implicated in numerous pathophysiological mechanisms, notably in the management of immune complexes or the recycling of autoantibodies. In humans, this role in the metabolism of autoantibodies has recently led to the development of therapeutic antibodies for autoimmune diseases such as autoimmune thrombocytopenia and myasthenia.
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, one of them being iNKT cells.
Studies in patients or in lupus mouse models have shown a decrease in iNKT cells correlated with disease activity as well as tissue infiltration in relation to clinical manifestations. Their actual role in this pathology remains to be clarified between regulatory or pro-inflammatory effect.
The possible role of iNKT as a regulatory cell in lupus pathology and the possible involvement of FcRn in their development reinforces the interest of their simultaneous study in humans.
The aim of this study will be to evaluate the impact of the expression of FcRn and other Fc gamma receptors cooperating with FcRn (Fc gamma RII and RIII) in iNKT cells in lupus patients in relation to disease activity and therapy. This study will be conducted in parallel on monocytes, cells involved in the metabolism of immune complexes and likely to be activated by iNKT cells. These results will be compared to healthy controls and integrated into mechanistic studies in a mouse model.
