Summary
The apoptotic signaling
pathway is obviously disordered in systemic lupus erythematosus (SLE).
Concurrent occurrence of induced apoptotic cell death and altered
phagocytosis promotes autoantigen production, which leads to the
biosynthesis of autoantibodies and autoimmune disorders. Natural IgM
(nIgM) is important in clearing apoptotic cells and preventing them from
triggering deleterious autoimmunity. B-1- and innate-like B- (ILBs)
cells are the main nIgM producers. Human
CD27+IgD+B cells (un-switched memory
B cells) are considered ILBs. However, their functional properties in
SLE remain undefined. Here, individuals with SLE showed markedly reduced
CD27+IgD+B cell amounts. Moreover,
these cells had altered function in terms of natural antibody-like IgM
production. CD27+IgD+B cells also
showed negative correlations with clinical and immunological properties
in SLE patients. Following effective treatment achieving SLE remission,
CD27+IgD+B cell amounts were
restored. Jointly, these findings suggest that
CD27+IgD+B cell dysfunction
potentially contributes to the exacerbation of SLE, and modulating their
features may represent a powerful tool for treating this persistent
disease.
Keywords: systemic lupus erythematosus,
CD27+IgD+ B cells, innate-like B
cells , natural IgM