Dysfunction of CD27+IgD+B cells correlates with aggravated systemic
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.