IIT-K, Univ of Queensland researchers find key molecules to help fight inflammatory diseases

Times News Network

Kanpur: The Indian Institute of Technology, Kanpur (IIT-K) and The University of Queensland (UQ) have published the results of a path-breaking international collaborative research on inflammatory diseases. The findings, published in ‘Molecular Cell’, a peer-reviewed scientific journal on molecular and cell biology, throw light on a protein receptor, C5aR2, that plays an important role in the moderation of many immune and inflammatory processes and explores its use as a potential therapeutic target for treating multiple chronic inflammatory diseases. The research witnessed international collaboration between IIT-K Professor Arun Shukla and Asuka Inoue of Tohoku University, Japan and Stéphane A Laporte of McGill University, Canada.

IIT-K claimed it to be the first time key molecules within the immune system have been identified which may help fight the inflammation leading to chronic inflammatory diseases. The findings will help further research in novel drug molecules that can act on the receptors for C5a, a potent immune molecule that is linked to immune-linked inflammatory diseases like cancer, rheumatoid arthritis, sepsis and even Covid-19.

Director, IIT-K prof Abhay Karandikar said, “We are optimistic that the findings of the research will lead to new light in the fight against chronic inflammatory diseases.”

University of Queensland, professor Trent Woodruff said that the research investigated the part of the immune system responsible for the body’s natural response to pathogens and injury, known as the ‘complement system’. He said, “When activated inappropriately, the system drives inflammatory diseases such as sepsis, COVID-19, stroke, heart attacks, cancers and brain illnesses. It’s been really challenging for researchers to understand how this protein is activated due to its unusual structure.”

“Instead of coupling with cell-signalling proteins, C5aR2 relies on signal regulating proteins known as β-arrestin proteins. Our study investigated interactions between the C5aR2 and β-arrestin proteins, while screening for molecules that activated a connection between the two. We found key and specific cell signals present when the C5aR2 was activated, which may boost the immune system’s response in inflammation,” added Prof Woodruff.

Co-investigator Professor Arun Shukla said the findings provided a framework for further exploration of β-arrestin proteins for their therapeutic modulation in disease. “We are now working to progress these research findings into disease models and potentially enable scientists to design novel drug molecules targeting C5aR2 to treat inflammatory disorders”.