Systemic lupus erythematosus – the autoimmune disease universally known as Lupus – afflicts at least 5 million people globally, according to National Resource Center on Lupus. Lupus can cause the body to attack its own tissue and can damage different organs – especially the kidneys, which suffer inflammation in roughly 50% of lupus patients.
While medications are available for lupus treatment, some patients’ bodies do not respond well to traditional treatment methods and they must undergo invasive treatments, such as dialysis or even a kidney transplant, which bring along additional side effects and can cause further damage to the body.
Researchers at Bar-Ilan’s Azrieli Faculty of Medicine sought to tackle this global issue and thus joined forces with teams from the Albert Einstein College of Medicine, the University of Houston, and the pharmaceutical company Equillium to develop a new targeted therapy. The study’s findings, which were published in the Journal of Clinical Investigation, show that the novel treatment inhibited specific immune cells and was effective in improving kidney inflammation in animal models.
Many different types of immune cells are involved in the mechanisms that target and damage organs in lupus – chief among them being T-cells, which affect the kidney by interacting and binding with other cells. T-cells containing the cell surface glycoprotein “CD6’ (the lock) bind with a molecule displayed on other cells known as ‘ALCAM’, causing T-cell activation and subsequent 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."
To prevent this damage from taking place, the researchers developed an antibody that disrupted the interaction between CD6 and ALCAM, preventing the T-cells from being activated. Fortunately, the blocking of the CD6/ALCAM pathway significantly therapeutic improved levels of kidney inflammation, and the researchers are moving forward on ways to use T-cell pathway disruption to treat lupus patients.