A new study provides hope for MS treatment with IGF-1, which could ultimately halt the attack of T effector cells on myelin, thereby stopping disease progression.
A new study provides hope for multiple sclerosis (MS) treatment.
According to the recent report, published in EMBO (European Molecular Biology Organization) Molecular Medicine, IGF-1 may be useful for treating autoimmune disease because it stimulates the proliferation of T regulatory cells.1 T regulatory cells are responsible for suppression of immune and inflammatory responses, and assist in the self-regulation of the immune system.
IGF-1 is a naturally occurring protein that causes cell division and protects from immune system-induced stress. Also known as somatomedin, it is already an approved medication, used to increase growth in people with certain types of dwarfism.
MS is characterized by the breakdown of myelin by the body’s own immune system, for reasons that are still not understood. With more than 2.3 million people affected by MS worldwide,2 treatments for MS are greatly needed. In autoimmune diseases such as MS, T-effector cells launch an immune attack on myelin. At the same time, T-regulatory immune cells also fail. T regulatory cells normally stop the T-effector immune response.
Investigators from the European Molecular Biology Laboratory (EMBL) in Monterotondo, Italy, examined both mouse and human T cells in vitro, and found that recombinant human (rh) IGF-1 increased the number of T regulatory cells when delivered via a miniature pump. The rhIGF-1 specifically affected T regulatory cells and not other immune cell types. The scientists also found that delivering rhIGF-1 into affected tissues in a mouse model of MS-known as experimental autoimmune encephalomyelitis (EAE)- increased T regulatory cells and suppression of immune responses specifically in the spinal cords of the animals. It also improved the movement problems that are normally induced in the EAE model.
In animals genetically modified to lack the IGF-1 receptor, the therapeutic effects of the rhIGF-1 were not observed, indicating that direct effects on the IGF-1 system are responsible for the T regulatory cell proliferation and other benefits.
The authors concluded that their study “shows that the protective action of exogenous rhIGFâ1 against autoimmune insults can be attributed to the direct stimulation of Treg cell proliferation.”
Treatment with IGF-1 could ultimately halt the attack of T effector cells on myelin, thereby stopping the progression of MS.
Because IGF is already approved and tested, clinical trials for IGF-1 may be relatively quick and easy.
1. Bilbao D, Luciani L, Johannesson B, et al. Insulin-like growth factor-1 stimulates regulatory T cells and suppresses autoimmune disease. EMBO Mol Med. 2014. pii: e201303376. doi: 10.15252/emmm.201303376
2. National MS Society Web site.
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