Cellerys and Immune tolerance

The physiological function of our immune system is to protect us from infectious agents and tumors. At the same time, it must not attack our body’s own cells and tissues, including cells that die by ageing. Tolerance mechanisms assure that dying cells do not lead to immune activation. Cellerys is developing therapies to reinstall immune tolerance in patients with autoimmune diseases such as multiple sclerosis.

Multiple sclerosis

Multiple sclerosis (MS) is a disease of the brain and spinal cord with chronic inflammation and widespread neurodegeneration. The root cause is a malfunction of the immune system. CD4+ T lymphocytes, also known as T helper cells, target specific self-antigens of the brain and spinal cord and cause an autoimmune response. The misdirected T cell attack against own brain or spinal cord tissue can lead to severe neurological damage. Approximately 2.5 million people worldwide suffer from MS.

Numerous approved therapies are available to treat MS. They are all either immunomodulatory or immunosuppressive and do not specifically target the autoimmune response in MS, but also impair normal protective immune functions with cord sometimes severe side effects. Most of the existing therapies need to be given for a long time.

  

The Cellerys approach

We are developing therapies that differ from existing MS treatments in autoimmune disease. Our approach is neither immunomodulatory nor immunosuppressive and aims at re-establishing immune tolerance. In other words, by mimicking our body’s physiological mechanisms, we induce and maintain tolerance to the body’s own tissues. Moreover, our therapies will leave the functioning of the immune system untouched.

Our approach has been examined in animal models and has been shown to be highly effective in both preventing and treating autoimmune disease.

Using this approach, Cellerys isdeveloping CLS12311 as a treatment for MS. The patient’s own red blood cells (RBCs) are collected, coupled with 12 peptides from 5 different target proteins associated with MS, and then given back to the patient. In the body, they are then degraded by the same physiological mechanisms as non-coupled aged RBCs. This process mimics the body’s own powerful mechanisms to remain tolerant against its own cells and at the same time against the target antigens coupled to their surface.