Scientists found a natural protein in immune cells, called CD72, that prevents the abnormal and damaging immune responses characteristic of autoimmune diseases, such as systemic lupus erythematosus (SLE).
Findings in the study, “CD72 negatively regulates B lymphocyte responses to the lupus-related endogenous toll-like receptor 7 ligand Sm/RNP,” recently published in The Journal of Experimental Medicine (JEM), may help in developing more efficient therapeutic strategies for SLE, and potentially other autoimmune disorders.
Previous work has shown that a protein called Toll-like receptor 7 (TLR7) plays an essential role in the development of SLE. Specifically, the TLR7 ligand called Sm/ribonucleoprotein (Sm/RNP; a ligand is a molecule that binds to a receptor) is a lupus self-antigen, meaning it activates immune cells to react against it. But the steps leading to these TLR7-mediated autoimmune responses remain unknown.
A team of scientists at Tokyo Medical and Dental University discovered that the CD72 protein, already known to block immune cell activation so as to prevent lupus development, actually works to shut down the autoimmune response.
The researchers found that CD72 recognizes the TLR7 ligand Sm/RNP. In this way, CD72 inhibits the binding between Sm/RNP and TLR7, which ultimately prevents the generation of autoantibodies, a crucial step in the development of lupus disease.
Scientists discovered the role of CD72 while working to understand how certain immune cells behaved when they removed (often called “knocked out”) CD72 from these same immune cells (B-cells, the cells in our immune system responsible for generating antibodies).
“When we knocked out CD72 in mouse B cells, they were specifically stimulated by the self-antigen Sm/RNP and released antibodies against this antigen,” said Takeshi Tsubata, with the Department of Immunology at Tokyo Medical and Dental University, and study’s senior author, in a press release. “The lack of CD72 meant that another receptor on B cells could bind to Sm/RNP, which activated the B cells and led to the symptoms of SLE.”
These results may well lead to a better understanding of autoimmune diseases, namely SLE, the scientists said.
“We now know that CD72 prevents immune responses which lead to SLE, without affecting responses to microbes and cancer cells,” Tsubata added. “If we can develop a method to augments capability of CD72, this will treat patients with SLE without unwanted effects.”
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