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.

Automated summary

This article discusses the role of CD8(+) T cells in the pathogenesis of SLE, highlighting how reduced cytolytic function of these cells promotes autoimmunity and contributes to organ damage, as well as the potential origin of pathological IL-17-producing double negative T cells from autoreactive CD8(+) T cells. Further research on the phenotypic changes of CD8(+) T cells is needed for the development of new therapeutics for SLE patients.