The development of lupus is accompanied by an accelerated accumulation of iron inside immune cells, molecular biologists from the United States have found. Suppressing this process in sick mice reduced the severity of autoimmune disease symptoms. The work was published in the journal Science Immunology, Vanderbilt University Press reported.

Systemic lupus erythematosus (SLE) is an autoimmune disease in which the immune system attacks the joints, skin, kidneys, blood cells, brain, heart and lungs. The most characteristic sign is a butterfly wing-like rash on the face. There is no cure for lupus yet, but treatment can help control the symptoms.

U.S. scientists studied intracellular processes in healthy and pathogenic forms of TH-17 cells and found that iron compounds were present in the immune cells of lupus carriers, even when the patients suffered from anemia.

The team studied how iron accumulates in pathogenic T cells and the consequences. The experiments showed that the main channel for iron entry is the cell receptor CD71. Its increased activity leads to the accumulation of iron in T cells and the development of their mitochondrial malfunction, as well as causing disruption of gene chains associated with inflammation.

Subsequent experiments on mice showed that suppressing CD71 with antibodies markedly reduced iron levels in T cells and the severity of lupus symptoms. This gives hope for drugs that will block iron accumulation in TH-17 cells of lupus carriers and protect them from developing severe symptoms of the disease.