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Improved Understanding of Damaging Immune Response in Rheumatoid Arthritis
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Improved Understanding of Damaging Immune Response in Rheumatoid Arthritis

Improved Understanding of Damaging Immune Response in Rheumatoid Arthritis
News

Improved Understanding of Damaging Immune Response in Rheumatoid Arthritis

Researchers within the Biomedicine Discovery Institute at Monash University have made a breakthrough in understanding the role played by high-risk immune genes associated with the development of rheumatoid arthritis (RA). Credit: (C) Erica Tandori.
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Researchers within the Biomedicine Discovery Institute at Monash University have made a breakthrough in understanding the role played by high-risk immune genes associated with the development of rheumatoid arthritis (RA).

The findings, published in Science Immunology, were the result of a seven-year collaboration led by Monash University, involving Janssen Biotech, Inc., Janssen Cilag Pty Ltd., Janssen Research & Development, LLC and the Karolinska Institute, Sweden.


Certain immune system genes, called Human Leukocyte antigen (HLA)-DR4, cause an increased susceptibility to RA.  In this study, using mice genetically modified to express the human HLA-DR4 molecule, the team examined, at the molecular and cellular levels, how T cells recognise these HLA-DR4 molecules. The team also showed that highly similar T cell receptors, likely with similar recognition characteristics, are also present in “RA-susceptible” humans expressing these HLA molecules.


“This suggests that there may be an immune signature of RA development, providing a potential avenue for diagnostic development or a window of opportunity for therapeutic development,” says Dr Hugh Reid, who co-led the study with Professor Jamie Rossjohn and Professor Nicole La Gruta at Monash University.

Reference
Lim JJ, Jones CM, Loh TJ, et al. The shared susceptibility epitope of HLA-DR4 binds citrullinated self-antigens and the TCR. Science Immunology. 2021;6(58). doi:10.1126/sciimmunol.abe0896



This article has been republished from the following materials. Note: material may have been edited for length and content. For further information, please contact the cited source.

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