Our immune system is armed with an array of defense designed to detect and eliminate harmful threats. One of its most powerful defense mechanisms is the complete system – A group of proteins that patrols our body, ever vigilant for signs or injury.

Now, 100 Years after the Complement System was first described, Researchers at Mass General Brigham has discovered Complement System Against Our Own Tissues.

Their findings not only reshepe the century-hour understanding of the complex system but also open new avenues for therapies that could spendly blocked Block this harmman Iseases. Results are published in Nature,

“Our discovery of a new way of activating the complex system, driven by an enzyme produced by cells that are abundant in inflamed tissues, have important clinical implices,” SAID LEAD AITHOR Ph.D., Instructor in Medicine at Harvard Medical School and A Postdoctoral Fellow in the Brenner Lab in the Division of Rheumatology, Inflammation, and Immunity at Brigham and Women’s Hospital, A Founding Member of the Mass Generaal Brigham Hathle Care.

“Our Work Highlights Gzmk as a Promising Therapeutic Target to Inhibit Complement Across Across Multiple Diseases. Unlike Traditional Therapies That Browdly Inhibit Consum ERVE The Anti-Microbial Functions of Complement, While Specifically Inhibiting This Harmful Pathway in Chronically Inflated Tissues . “

The work, carried out in the laboratory of Michael Brenner, MD the Ef Brigham Professor of Medicine at Harvard Medical School, was driven by a Compeling ObServation The Brener Group Had Made EARLIARERERERERERE^, T cells in the inflated synovium of rheumatoid arthritis patiants –nd in affected organs Across Various Inflammatory Diseases – Produud Gzmk, A Protein That Had Ann UNCLER Function.

Intriguingly, other research groups have also Iduals. Given their widespread abundance in inflamed tissues, the research team suspended that these cells –nd gzmk -might play a fundamental role in driving inflammatory damage.

To explore this, they are analyzed the protein sequence of gzmk and compared it to other human proteins to find clohes about its function. Through a series of experiences, they demonstrated that gzmk activated the entrepreneurous complement Cascade, Producing Complexities that Drive Inflammation, Recruit Immune Cells, and Cause Tisse Tisse Tisse TisSue Damage.

Their research further revised that in human rheumatoid arthritis synovium, gzmk is enriched in regions exhibiting Abundant Complement Activation. In Two Independent Animal Models of Rheumatoid Arthritis and Psoriasiform Dermatitis, Mice With a Gnetic Deficiency in Gzmk Were Significly Protected from Disease , And Complement Activation – Compared to Mice With Normal Gzmk Expression.

“These Findings Underscore The Pivotal Role of Gzmk-Deedated Complement Activation in Driving Disease and Highlight The Broad Translational Potanical of Targeting This Pathway Accounts Multiple Disease States,” Erin Theisen, MD Ph.D.

“Our Findings Provide New Insights Into How Chronic Inflammation Might be triggered and sustained in autoimmune and inflammatory diseases,” said Senior Author Michael Brener, md.

“Moving Forward, We will continue to investigate the impact of this pathway across varous diseases and area work S Suffering from autoimmune and inflammatory conditions. “