Do naturally occurring autoantibodies participate in the constitution of the pathological B-cell repertoire in systemic lupus erythematosus?
Systemic lupus erythematosus (SLE) is the prototype of systemic autoimmune diseases. In both human and mouse SLE diseases, the autoimmune response targets a restricted set of autoantigens. Many of them are nucleic acids and proteins involved in the synthesis and processing of DNA or RNA, a characteristic which should be taken into consideration to elucidate the origins of non organ-specific autoantibodies. Several observations, in particular those obtained from experimental models of SLE induced in normal mice, suggest that the breakdown of B-cell tolerance occurs in the periphery. Herewith, we present data further supporting the proposition that SLE-associated autoantibodies originate from natural autoantibody-secreting B cells activated in the internal environment of lupus mice. Thus, one may hypothesize that certain clones of the expanded primary B-cell repertoire are selected to differentiate into harmful IgG autoantibody-secreting clones, thereby raising the question of the nature
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