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Blocking a specific cell immune messenger can reduce the effects of the most common type of arthritis from progressing, according to new research undertaken at Xi’an Jiaotong-Liverpool University.
The Sacitharan Lab at XJTLU, working with other labs across China, has found that the targeting of an immune messenger, called IL-33, stops osteoarthritis progression.
Half of the world’s population aged 65 years or older suffers from osteoarthritis, the most common form of arthritis. In osteoarthritis, the cartilage over the ends of bones in joints breaks down and the bones rub together, causing pain, swelling and loss of motion.
Despite its prevalence, this form of arthritis does not have effective treatments, with joint replacement surgery a costly option and not effective for smaller hand joints and spine osteoarthritis.
Dr Pradeep Kumar Sacitharan of XJTLU'sDepartment of Biological Sciencesexplained the value of this research.
“To date, finding a treatment for osteoarthritis has been difficult. There is an urgent need to find suitable drug targets to address both disease pathogenesis and pain,” he said.
“We were struggling to find which cells in the different types of tissues of a joint can be producing signals to cause the disease.
“The immune system’s role in the puzzle was largely ignored until now, but what our researchers have found is that IL-33 [a cytokine: protein important in cell messaging] is produced from only one type of cell in the joint which can lead to novel precision targeted medicines.
“Blocking IL-33 may be a potentially new method to stop osteoarthritis and its related pain.”
Dr Sacitharan added that further human trials are still required.
“This data shows us that we can target one messenger from one cell type to stop the disease and its related pain, which is good news for patients. However, we need to conduct further clinical trials.”
The research, 'Blockade of IL‐33 signalling attenuates osteoarthritis', was recently published inClinical & Translational Immunology(CTI).
The research also recently featured as aresearch highlightinNature Reviews Rheumatology.
ByWill Venn
Social media editor:Xiaowan Yuan, Qifan Yu
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