The term “autoimmunity” describes the inability of the human body’s immune system to recognize its own cells and tissues as its own, instead launching immune attacks against these cells and tissues as if they were foreign or invading.
Advances in medical research on the immune system have revealed links between inflammation and many conditions. Understanding how the immune system is activated and regulated is essential for patients with symptoms suggestive of autoimmune diseases, for researchers developing treatments for autoimmunity, chronic inflammation, and allergies, and for those applying these treatments in clinical practice.
Recently, researchers from the Stanford and Yale Schools of Medicine, together with specialists from the Research Institute of the Hospital for Special Surgery in the United States, discovered new information about how the immune system prevents the production of antibodies that could damage the healthy tissues of the organism.
A study published in the Journal of Experimental Medicine (JEM) on September 29 reveals how this process is affected in autoimmune disorders such as systemic sclerosis and systemic lupus erythematosus, and suggests potential new strategies for treating these diseases.
B cells are a type of white blood cell that help fight infection by producing antibodies capable of recognizing foreign molecules called antigens produced by invading pathogens such as bacteria and viruses. However, some B cells produce antibodies that recognize “autoantigens” produced by the body’s own cells, which can cause the immune system to mistakenly attack healthy tissue, causing a variety of autoimmune diseases.
To prevent this, the immune system tries to eliminate autoreactive B cells by exposing them to autoantigens as they develop in the bone marrow. This process, called central-type immunological tolerance, is thought to be controlled by B-cell receptors (BCRs) on the surface of developing B cells. B cells with BCRs that bind to autoantigens are eliminated before they can leave the bone marrow and enter the circulation.
The new JEM study, led by research teams led by Eric Meffre of Yale University School of Medicine and Franck J. Barrat of the Hospital for Special Surgery in New York, shows that central tolerance also depends on a receptor called TLR9 . This receptor is found inside B cells in compartments called late endosomes and is activated by binding to fragments of DNA.
The researchers found that depletion of TLR9 impairs central tolerance and leads to increased production of autoreactive B cells and antibodies in mice. They also observed that TLR9 activity is reduced in B cells from patients with systemic sclerosis and lupus, both of which are autoimmune diseases.
The reduction in TLR9 activity is due to a protein called CXCL4, which, like TLR9, can bind to fragments of DNA. High levels of CXCL4 have been observed in patients with these diseases, and the protein prevents the delivery of DNA fragments to late endosomes, where they should activate TLR9 and induce B-cell tolerance.
The results of this study suggest that correcting defective TLR9 function in B cells of patients with autoimmune diseases, potentially by neutralizing CXCL4, could represent a new therapeutic strategy for restoring B cell tolerance.
Source: 360medical.ro
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2023-10-03 06:48:44
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