Researchers from the Karolinska Institute, Sweden report that antibodies that exist in the joints before the onset of rheumatoid arthritis can cause pain in the absence of arthritis—they recently reported their findings in the Journal of Experimental Medicine. They believe the finding can represent a general mechanism in autoimmunity and that the results can help contribute to the development of new ways of reducing non-inflammatory pain caused by rheumatoid arthritis and other autoimmune diseases, reports MedicalXpress.
An immune disease that occurs when immune cells attack the cartilage and bone of the joints. The disease affects roughly one percent of the Swedish population reports MedicalXpress.
Joint pain is a common early symptom, but before that point, the body already starts producing immune antibodies against proteins in the joint. The Swedish research team has been intensely studying how these autoantibodies can generate pain.
The team injected cartilage-binding autoantibodies into mice, which served as a model for human rheumatoid arthritis, the researchers found that the mice became more sensitive to pain, even before they could observe any signs of inflammation in the joints. The antibodies had been designed not to activate immune cells and trigger inflammation also induced pain-like behavior in the mice—pointing toward increased pain sensitivity in the joints as reported in MedicalXpress.
Antibodies that caused behavioral change form so-called immune complexes, comprising clusters of antibodies and cartilage proteins in the joints. These immune complexes trigger pain cells via “Fc-gamma receptors” which the Swedish team uncovered on pain neurons in the tissue. Follow the link below to the source for more details.
Camilla Svensson, Professor Department of Physiology and Pharmacology, Karolinska Institute