Contributions of B cells to lupus pathogenesis

Abstract

Systemic lupus erythematosus (SLE) is an autoimmune disease characterized by the production of autoantibodies. This review summarizes first the results obtained in the mouse that have revealed how B cell tolerance is breached in SLE. We then review the B cell subsets, in addition to the autoAb producing cells, which contribute to SLE pathogenesis, focusing on marginal zone B cells, B-1 cells and regulatory B cells. Finally, we review the interactions between B cells and other immune cells that have been implicated in SLE, such as dendritic cells, macrophages, neutrophils and T cells.

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“…Kes., Ph.D., Apt, Faculty of Pharmacy, Universitas Airlangga, 4 -6 Airlangga Road, Surabaya -6 0115, Indonesia. E-mail: junaidi-k@ff.unair.ac.id be shedded in the circulation become the memory T cells 9,10 . The low number of L-selectin in the spleen will increase the lupus severity since the high number of T effector, some of them are autoreactive, cannot be handled results in inflammation.…”

Unexpected Potency Differences between B-Cell-Activating Factor (BAFF) Antagonist Antibodies against Various Forms of BAFF: Trimer, 60-Mer, and Membrane-Bound

“…These autoantibodies form pathogenic immune complexes that deposit into organs, ultimately inducing inflammation and tissue damage (Cancro et al, 2009;Sang et al, 2014). Many of the current therapeutic options for the treatment of SLE include antimalarial agents, nonsteroidal anti-inflammatory drugs, glucocorticoids, and immunosuppressive drugs, which all seek to reduce the autoimmune inflammatory process but also can result in general immunosuppression and toxicity (Tsokos, 2011).…”

A brief insight into systemic lupus erythematosus pathogenesis

“…Studies on murine models revealed abnormal signaling mechanisms through B lymphocytes, with the AKT/mTOR pathway playing an essential role [19,20]. The gene analysis of signaling molecules specific for B lymphocytes identified two inhibitor receptors, Lyn and CD22, which are critical in the regulation of B lymphocyte phenotype expressed in SLE.…”