The role of CD8+ T-cell systemic lupus erythematosus pathogenesis: an update

Purpose of review Systemic lupus erythematosus (SLE) is a serious autoimmune disease with a wide range of organ involvement. In addition to aberrant B-cell responses leading to autoantibody production, T-cell abnormalities are important in the induction of autoimmunity and the ensuing downstream organ damage. In this article, we present an update on how subsets of CD8(+) T cells contribute to SLE pathogenesis. Recent findings Reduced cytolytic function of CD8(+) T cells not only promotes systemic autoimmunity but also accounts for the increased risk of infections. Additional information suggests that effector functions of tissue CD8(+) T cells contribute to organ damage. The phenotypic changes in tissue CD8(+) T cells likely arise from exposure to tissue microenvironment and crosstalk with tissue resident cells. Research on pathogenic IL-17-producing double negative T cells also suggests their origin from autoreactive CD8(+) T cells, which also contribute to the induction and maintenance of systemic autoimmunity. Reduced CD8(+) T-cell effector function illustrates their role in peripheral tolerance in the control of autoimmunity and to the increased risk of infections. Inflammatory cytokine producing double negative T cells and functional defects of regulatory CD8(+) T cell both contribute to SLE pathogenesis. Further in depth research on these phenotypic changes are warranted for the development of new therapeutics for people with SLE.