Although there currently is no cure for the disabling neurological disease multiple sclerosis (MS), findings from a new Johns Hopkins Medicine study provide strong support for a promising advance toward that goal: the ability to reverse — and in many cases, completely alleviate — MS-like symptoms in mice.

For an unknown reason in people with MS, some of the body’s first line of defense against foreign invaders — immune cells known as CD4+ T cells — fail to recognize that myelin (which surrounds and protects nerve cells) is a normal part of the human system. If these wayward, or effector, T cells become dominant, they may provoke inflammation that damages or destroys the myelin sheath, which, in turn, can severely disrupt or curtail transmission of nerve impulses from all parts of the body to the brain.

“We developed a method for ‘tipping the balance’ of the T cells reaching the central nervous system from effectors to regulatory T cells, or T regs, that modulate the immune system and have been shown to prevent autoimmune reactions,” says Giorgio Raimondi, assistant professor of plastic and reconstructive surgery, and co-senior author of a study appearing in Science Advances.

“Using this therapy on mice bred to exhibit symptoms modeling those seen in humans with MS, we found we could enhance the growth of T regs while simultaneously reducing the number of effectors, resulting in reversal of the MS-like symptoms in 100% of the mice, and even more exciting, achieving a full recovery in 38% — in other words, more than a third were cured of their disease,” says Raimondi, associate director of the Vascularized Composite Allotransplantation Research Laboratory.

The researchers achieved these intriguing results by using biodegradable polymeric microparticles — tiny, bioengineered polymer spheres — to deliver three key therapeutic agents.

Along with further studies to confirm the effectiveness of their potential MS therapy, Raimondi and colleagues plan to try their microparticle therapy delivery system on other autoimmune diseases.

First in line? A mouse version of type 1 diabetes. “To engage and grow T regs specific for the insulin-producing cells in the pancreas damaged or threatened by that disease’s autoimmune activity, we’ll exchange the myelin peptide we used in the MHC-peptide portion of the MS therapy with one from those cells,” says biomedical engineer Jamie Spangler, study co-senior author.