Cytokine Gene Expression in Human Systemic Lupus Erythematosus

Abstract

Genetic background and environmental factors predispose to, and may contribute to the aberrant immune regulation that characterizes systemic lupus erythematosus (SLE). Identifying additional predisposing factors could elucidate pathogenic mechanisms, and help stratify and devise targeted therapy for this complex disease. Cytokines are hormone-like glycoproteins that form an interrelated network of additive, synergistic, or antagonistic activities, and are essential for the regulation of immune/inflammatory responses. Cytokines bind to cell membrane-anchored receptors, associated with signal transducers and activators of transcription (STAT) molecules, that, on activation, translocate to the nucleus and induce gene transcription. Following cell activation, cytokine receptors may be secreted into the extracellular milieu as truncated molecules lacking cytoplasmic and/or transmembrane domains that either can interfere with cytokine binding to the membrane-anchored receptors or, by contrast, may transport and deliver cytokines to their high-affinity membranal receptors.