Introduction: T cells and systemic lupus erythematosus

erythematosus Systemic lupus erythematosus (SLE) is an autoimmune disease that affl icts mainly women in the reproductive years. It is a multisystem disease aff ecting the joints, skin, kidneys and brain and is characterized by autoantibody production by dysregulated B cells, target organ infi ltration by infl ammatory T cells and aberrant immune cell activation due to abnormal antigen presenting cell (APC) function. While aberrant T cells provide help to auto reactive B cells, they also infi ltrate target organs, caus ing damage, and thus are key players in SLE disease patho genesis. Understanding the underlying defects within T lymphocytes is of utmost importance not only for understanding disease pathophysiology, but also for identifying predictive biomarkers and better therapeutic targets. T lymphocytes from SLE patients are unique in that they resemble naïve or somewhat anergic T cells in certain ways, such as their reduced ability to produce cytokines like interferon-γ and IL2, but simultaneously bear characteristics reminiscent of activated/memory T cells, such as the overall increased tyrosine phosphorylation of signaling intermediates, accelerated calcium fl ux responses, altered expression of signaling subunits such as the T cell receptor (TCR) zeta and FcRγ, and expression of adhesion or costimulatory molecules such as CD44 and CD40L. Th e following sections describe in detail these and other T cell signaling abnormalities that are responsible for their defective phenotype and function and may potentially contribute to disease pathogenesis.