Targeting iron metabolism in immune system cells could be a potential new approach for treating systemic lupus erythematosus (SLE), the most prevalent form of the chronic autoimmune disease lupus. Researchers from Vanderbilt University Medical Center recently published their findings in the journ
Lupus is a chronic autoimmune disease in which the body’s immune system attacks its own healthy tissues and organs. This results in inflammation and damage to various parts of the body, including the skin, joints, kidneys, heart, lungs, brain, and blood cells.
Treatments for lupus aim to control symptoms, reduce immune system attack of tissues, and protect organs from damage. Only one targeted biologic agent has been approved for treating SLE, belimumab in 2011. Rathmell’s group has had a long-standing interest in lupus as part of a broader effort to understand the mechanisms of autoimmunity.
To explore T-cell iron metabolism in lupus, Voss and Rathmell drew on the expertise of other investigators at VUMC:Amy Major, Ph.D., and her group provided a mouse model of SLE; andFirst, Voss used a CRISPR genome editing screen to evaluate iron-handling genes in T cells. She identified the transferrin receptor, which imports iron into cells, as critical for inflammatory T cells and inhibitory for anti-inflammatory regulatory T cells.
An antibody that blocks the transferrin receptor reduced intracellular iron levels, inhibited inflammatory T cell activity, and enhanced regulatory T cell activity. Treatment of SLE-prone mice with the antibody reduced kidney and liver pathology and increased production of the anti-inflammatory factor, IL-10.
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