Lupus: a new study improves our understanding how this disease is prevented in healthy individuals

Systemic lupus erthematosus (SLE) is a disease associated with inflammation of various organs including kidney, brain, skin, heart and lung, due to body’s immune system attacks its own cells mistakenly.  In a major breakthrough in the fight against this disease, a team of researchers at Tokyo Medical and Dental University (TMDU) have identified a molecule which stops the immune system from attacking components of body’s own cells. With this study provides the explanation of mechanism that develops the disease, it could greatly enhance our ability to treat this condition.

Current treatments just address the symptoms while there is no cure for lupus. As a result people with lupus face increased risk of infection and metabolic diseases due to treatments. With the finding, a molecule that prevents immune cells from reacting with the body and causing SLE and explanation of the mechanism behind its action has raised the hopes of treatments of this disease.

The natural function of immune cells is to recognize potentially damaging agents such as toxins, cancerous cells, and bacteria and viruses. In order to neutralize and remove such agents from body immune cells release proteins called antibodies that can specifically identify these agents elsewhere in the body. Sometimes this natural function goes awry, leading immune system to attack healthy cells or tissues of the body.

Past research has identified some cells and molecules that could be involved in this condition but exact mechanism behind its action was not clear; therefore giving no idea how to prevent its development in healthy individuals. Building on past studies, a team at TMDU have identified a molecule called CD72 that prevents a certain type of immune cell from mistakenly reacting with a protein complex within the body.

"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," says Takeshi Tsubata of the Department of Immunology at TMDU. "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."

To establish the authenticity of their findings, the team analyzed different variants of CD72 and found that these variants differed in their potency of preventing development of SLE.

"We now know that CD72 prevents immune responses which lead to SLE without affecting responses to microbes and cancer cells," Takeshi Tsubata of TMDU says. "If we can develop a method to augments capability of CD72, this will treat patients with SLE without unwanted effects."