Introduction

Based on the discovery of a novel pathogenetic mechanism involving p75NTR receptor, authors demonstrated that p75NTR receptor inhibitors, alone or in association with TrkA receptor activators,  reduce inflammatory cytokine production and prospect their use for anti-inflammatory treatment of  chronic inflammatory diseases of auto-inflammatory or autoimmune origin.

Technical features

Chronic inflammatory diseases are characterized by inflammation leading to tissue damage and loss of target tissue function. Current therapies are based on not steroidal anti-inflammatory drugs, cortisone based and immunosuppressive drugs, but are effective only for a low percentage of patients and are side-effect burdened. It is therefore apparent the need to provide for new therapies for treatment and prevention of such diseases. CNR and OBPG researchers demonstrated that high p75NTR and anomalous p75NTR/TrkA ratio characterize chronic inflammatory disease patients and positively correlate with inflammatory parameters and clinical symptoms. p75NTR activation in patient cells enhances the production of  pro-inflammatory  cytokines while its inhibition drastically reduces  their synthesis prospecting p75NTR as a new target for therapeutic approaches for chronic inflammatory diseases of autoinflammatory or autoimmune origin.

Possible Applications

Chronic inflammatory diseases of autoinflammatory or autoimmune origin such us:
rheumatoid arthritis, juvenile idiopathic arthritis, intestinal chronic inflammatory diseases, ankylosing spondylitis, psoriasis, multiple sclerosis, juvenile dermatomyositis, Lupus erythematosus, scleroderma, Syndrome of Sjogren.

Advantages

• Reduction of the production of several proinflammatory cytokines
• Shift of the balance towards the activation of TrkA-mediated anti-inflammatory pathways
• Applicability in a wide range of diseases