New Israeli Therapy Helps Patients With Lupus Disease

A new, targeted therapy inhibits specific immune cells associated with lupus nephritis, bringing hope to sufferers.

By Pesach Benson, United With Israel

Israeli researchers have developed a breakthrough treatment that could help people suffering from lupus nephritis, a disorder in which the immune system attacks the body’s kidneys.

According to the Lupus Foundation of America, at least five million people worldwide have some form of lupus, which can also attack the brain, joints and skin. Its estimated that half of all lupus sufferers have lupus nephritis.

Available treatment can effectively treat lupus nephritis. However, not all people respond well to the treatment because the medications involved suppress the immune system, making patients highly susceptible to infection. A patient whose kidneys reach a certain point of scarring or inflammation will require dialysis or a kidney transplant to stay alive. Treatment is further complicated by the fact that other organs are under attack.

A new, targeted therapy, developed by researchers from the Azrieli Faculty of Medicine of Bar-Ilan University, the Albert Einstein College of Medicine, the University of Houston, and the pharmaceutical company Equillium, together with several other academic collaborators, inhibits specific immune cells associated with lupus nephritis.

This therapy was found to be effective in improving kidney inflammation in animal models of lupus and lupus nephritis. The new approach could serve as an alternative to current treatments targeting multiple immune cells and provide a more effective and potentially personalized remedy for lupus nephritis. The development was reported in a study published in the Journal of Clinical Investigation.

Many different types of immune cells are involved in the mechanisms underlying target organ damage in lupus and other autoimmune conditions. Among these important cell types are T-cells, which affect the kidney by interacting and binding with other cells, similar to a key being inserted into a lock. The researchers found that the T-cells expressing a glycoprotein called CD6 (the lock) would bind with a molecule known as ALCAM that is displayed on other cells (the key). When this binding was complete, the T-cells would activate, leading to kidney inflammation.

To prevent this damaging development, the researchers developed an antibody that disrupted the process by blocking the interaction between CD6 and ALCAM. It’s the equivalent of pouring glue into a lock to prevent any key from unlocking it.

When activation of the CD6/ALCAM pathway was blocked in animal models, the researchers observed significant therapeutic improvement in kidney inflammation.

“Up until now, CD6/ALCAM interactions weren’t considered relevant or instrumental in lupus nephritis,” says Prof. Chaim Putterman, of the Azrieli Faculty of Medicine of Bar-Ilan University (Safed, Israel) and the Albert Einstein School of Medicine (Bronx, NY), who led the study together with senior co-authors Dr. Cherie Ng and Dr. Chandra Mohan.

“The intervention we describe, which targets T cells rather than multiple immune cell types, can potentially provide physicians with another effective tool for treatment of a difficult and challenging disease.”

Symptoms of lupus nephritis include weight gain, fatigue, high blood pressure, fever, a red rash, pain in the joints, frequent urination, blood in the urine and swelling in the legs, feet, ankles, joints, hands or face.