Called APC cells, an acronym for Antigen-Presenting Cell, or “cells that present the antigen,” dendritic cells (DC) once activated migrate to the lymph nodes where they push the T and B cells of the immune system to trigger the reaction. In rheumatoid arthritis the process “goes haywire,” and instead of defending the body these cells are pushed to attack the tissues of the joints, organs, and bones, also producing pathological antibodies.
By isolating dendritic cells from the synovial fluid, blood and joints of some patients with rheumatoid arthritis, researchers have discovered that in addition to developing inflammatory molecules, they are rich in MiR34a, especially in those in the early stages of the disease. This molecule is able to suppress another molecule that regulates the action of dendritic cells, AXL, which is deficient in patients with rheumatoid arthritis. Using this knowledge in some experiments on mice, scientists have discovered that by suppressing MiR34a, the animals are able to develop a real resistance to rheumatoid arthritis.
Through targeted drugs – some of which are already being tested – capable of inhibiting this molecular switch in humans too, it will therefore be possible to “re-establish the immunological balance and promote the resolution of arthritis”, as Professor Ferraccioli optimistically underlined.
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