Dysfunction of CD27+IgD+B cells correlates with aggravated systemic
lupus erythematosus
Abstract
Apoptotic signaling pathway is obviously disordered in systemic lupus
erythematosus (SLE). The contemporaneous occurrence of enhanced
apoptosis and impaired phagocytosis lead to the cumulative exposure to
autoantigens, resulting in autoantibody production and autoimmunity.
Natural IgM (nIgM) plays a key role in the clearance of apoptotic cells
and prevents them from inducing abnormal autoimmunity. B-1 cells and
innate-like B cells (ILBs) are proved to be the major producer of
natural IgM. Human CD27+IgD+B cells, also termed as un-switched memory B
cells, are recently proposed to be a kind of ILBs. However, functional
features and characteristics of these cells in SLE remain poorly
understood.In this study, we find that in SLE patients the frequencies
of CD27+IgD+B cells are significantly decreased. Moreover, these cells
are functionally impaired in producing natural antibody-like IgM. These
CD27+IgD+B cells are negatively correlated with SLE patient clinical and
immunological features. After effective therapy with disease remission
in SLE, the frequencies of these cells could be recovered. Taken
together, our results suggest that the dysfunction of CD27+IgD+B cells
potentially contribute to the exacerbation of SLE, and modulating the
features of these cells might provide therapeutic target for this
persistent disease.