Unmet Need
Hundreds of thousands of patients worldwide are affected by inflammatory diseases caused by a preexisting condition (inflammatory arthritis, psoriasis) or rejection of a foreign body (medical implant, open wounds). This is caused by the over/underexpression of certain phenotypes of macrophages within patients, yielding a disruption in homeostasis of tissue cells and an aggravated immune response, often resulting in fibrosis – a formation of excess fibrous tissues around the affected area. Patients are often treated using NSAIDs, corticosteroids, and other anti-inflammatory drugs, which can be cumbersome and ineffective. There is a critical need for identification and targeting of specific macrophage phenotypes responsible for the exaggerated immune response resulting in fibrosis.
Technology Overview
A new in silico method of classifying macrophages through a combination of surface markers has prompted the discovery of a unique gene expression in the macrophage cluster F2. Certain genes’ characteristic expression in fibrotic environments has led researchers to conclude that these genes are responsible for driving fibrosis in affected patients. Thus, the targeting and inhibition of the macrophage F2 cluster could halt and possibly reverse the effect of fibrosis in patients. Though no specific method of targeting has been chosen, potential therapeutic routes include gene editing, RNAi, Ab, and surface coatings. This approach offers a possible effective and long-term solution to a wide variety of conditions including arthritis and tumor formation.
Stage of Development
There have been several in vivo and in silico experiments conducted using biomaterials and biologic scaffolds to prove F2 cluster’s role in fibrosis.
Publications
https://www.biorxiv.org/content/10.1101/642389v1
