On pp. 47–57 of this issue, George Tsokos and colleagues present a Feature review on the pathogenesis of human systemic lupus erythematosus (SLE), an autoimmune disease involving multiple organs including the kidneys, joints, nervous system, and hematopoietic organs. The heterogeneity of the disease and lack of adequate tools to diagnose and follow disease progress have been obstacles in the development of effective therapies. The authors discuss the cellular and molecular alterations in the immune system in patients with SLE. Recent findings include the identification of genes associated with disease expression, immune cell dysfunctions that lead to autoimmune pathology, the role of hormones and sex chromosomes in disease development, and environmental and epigenetic factors that might contribute to the expression of SLE. The authors explain how the immune system is broadly compromised in patients with SLE, and that deregulation of specific elements can lead to altered behavior of the whole system. Finally, they discuss the key molecular defects associated with pathogenesis that might represent therapeutic targets and disease biomarkers. Cover image: T cells from SLE patients produce increased amounts of pro-inflammatory cytokines such as IL-17. The image shows T cells from a patient with SLE, stimulated with anti-CD3 and anti-CD28, and stained with anti-IL-17 (green) and nuclear dye DAPI (blue) after permeabilization. Cover image provided by George Tsokos.

Trends in Molecular Medicine 2008 Impact Factor: 9.621
*Source: 2008 Thomson Reuters JCR

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