Abstract:

ABSTRACT long-lived plasma cells can secret antibodies to participate in permanent immunity, and can produce autoantibodies in autoimmune diseases, such as systemic lupus erythematosus (SLE), which make it deferral and relapse. Survival niches for long-lived plasma cells are provided by bone marrow, and in morbid state also by spleen and inflamed tissues, where survival signal factors are exist, and the down-regulation of many cell surface markers may also contribute to the reason of long-living. Nowadays, drugs used to treat SLE often target to short-lived plasma cells, and can’t delete long-lived plasma cells. The identification of some of the factors involved in the pathways has permitted the development of specific therapeutic approaches and may even provide investigators with further new therapeutic targets, particularly in autoimmune diseases associated with persistent autoantibody production. Some immunosuppressive agents like Bortezomib can eliminate long-lived plasma cells.

Key words: long-lived plasma cells, Systemic lupus erythematosus