Researchers discover that a molecule of blood is effective against autoimmune kidney disease

Lupus is a chronic autoimmune disease that can damage any part of the body. When it causes inflammation in the kidneys (called lupus nephritis), they cannot properly remove waste from the blood or control body fluids. Without treatment, nephritis can lead to scarring and permanent damage of the kidneys, and possibly final renal failure. In this case, patients need to undergo dialysis and possibly a kidney transplant. Currently, lupus nephritis patients are treated with nonsteroidal anti-inflammatory drugs and immunosuppressors, which are unsatisfactory and have side effects. Therefore, new therapeutic agents with higher potency, selectivity and safety are needed.

The research group, on immuno-inflammatory processes and gene therapy of the Bellvitge Biomedical Research Institute (IDIBELL), has published a study in the prestigious journal Kidney International that demonstrates the immunomodulatory therapeutic capacity of a molecule present in our blood, called C4BP (β-). These results, validated in two animal models of lupus nephritis, represent a very promising advance for patients. Also, the applicability of this discovery is being evaluated in other autoimmune disorders, such as colitis and rheumatoid arthritis.

Autoimmune diseases are caused by a malfunction of the immune system, which attacks its own cells and tissues, becoming an aggressor instead of a protector. The complement pathway is one of the components of the innate system. This, among other functions, protects the body from pathogenic organisms. The IDIBELL team, led by Dr. Josep M. Aran, has demonstrated a new activity for one of the forms of complement inhibitor protein C4BP (β-). Specifically, it has been shown that the protein is able to reprogram myeloid cells (a type of white blood cell), transforming its proinflammatory and immunogenic activity to anti-inflammatory and tolerogenic activity.

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