The pathogenesis of systemic lupus erythematosus-an update

Abstract

Systemic lupus erythematosus (SLE, lupus) is characterized by a global loss of self-tolerance with activation of autoreactive T and B cells leading to production of pathogenic autoantibodies and tissue injury. Innate immune mechanisms are necessary for the aberrant adaptive immune responses in SLE. Recent advances in basic and clinical biology have shed new light on disease mechanisms in lupus, with this review discussing the recent studies that offer valuable insights into disease-specific therapeutic targets.

Mechanism of autoantibody production and tissue injury in lupus: A paradigm

Self-antigen dependent activation of autoreactive B cells and CD4 T cells in secondary lymphoid organs, leads to production of pathogenic autoantibodies that, along with inflammatory cytokines, promotes tissue injury in lupus. Antigen-presenting dendritic cells are necessary for adaptive immune cell activation, and contribute to inflammatory cytokine production. Autoantibodies in complexes with autoantibodies contribute to innate immune cell activation and cytokine production. Genetic predisposition is a requisite for aberrant immune system acivation, in the setting of environmental and stochastic events. Abbreviations: DC, dendritic cells; pDC, plasmacytoid dendritic cells.