Summary
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.
Keywords: systemic lupus erythematosus, innate-like B cells,
CD27+IgD+ B cells, natural IgM