Lupus is a chronic, autoimmune disease that causes inflammation, particularly of the skin, joints, blood, and kidneys. Patients with lupus produce antibodies against their own proteins. Patients also have immune T cells that produce a protein called IL-2, which normally usually protects against infection, at lower than typical levels. In a study appearing in the April 1 print edition of The Journal of Clinical Investigation, George Tsokos and colleagues from the Walter Reed Army Institute of Research explore the mechanisms underlying this decreased IL-2 production.
The researchers find that sera from lupus patients contains antibodies that bind to T cells and activate a complex cellular signaling cascade that ultimately results in decreased IL-2 production. This deficiency in IL-2 could result in the autoantibody production that occurs in lupus.
In an accompanying commentary, Gary Kammer of Arthritis Associates, Inc points out "the contribution by Tsokos and his colleagues…provides a new appreciation and insight into how the microenvironment in lupus can further impinge on a defective T cell to inhibit IL-2 production. From such studies will come the inspiration and novel approaches necessary to develop therapeutic tools to abate disease and improve the quality of life of our patients."
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