A clotting disorder’s immune origins

Immune thrombocytopenia (ITP), a bleeding disorder characterized by low blood platelet numbers, can result in excessive bleeding during injuries.

While ITP is known to be an autoimmune disorder, the precise mechanisms of both the disease and a common treatment, intravenous immunoglobulin (IVIG) administration, have been unclear.

In a study published on July 10 in Science Translational Medicine, Kavita Dhodapkar, MBBS, associate professor of pediatrics, and colleagues detail the unique genetic signature of children with ITP. They show that this signature is mediated by elevated levels of both infection-fighting proteins called interferons and innate immune cells called plasmacytoid dendritic cells found in ITP patients.

The research team also showed that IVIG treatment diminishes the elevated gene expression, but only temporarily, a finding that is consistent with the treatment’s short-lived efficacy. These studies therefore provide potential targets for new therapies against ITP by directly attacking the underlying innate immune cells.


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