Identification of Immunomodulatory Cells Induced By 670 nm Light Therapy in an Animal Model of Multiple Sclerosis

Abstract

Multiple sclerosis is an autoimmune, demyelinating disease characterized by neurodegeneration and inflammation of the central nervous system. It affects approximately 250,000 people in the United States alone, with women being affected two times more than men. Experimental Autoimmune Encephalomyelitis (EAE) is the primary animal model of MS, sharing clinical signs and histopathology with MS. The current paradigm supports MS/EAE induction by myelin reactive CD4+ T cells that cross the blood brain barrier to induce an inflammatory response that leads to the destruction of the myelin sheath and eventual loss of axons. Recent data suggest that axonal loss and disease progression are due to accumulation of oxidative stress. Most of the current therapies for MS are only useful early in the disease process, slowing disease progression but not preventing it, probably because they do not affect oxidative stress. With previous studies showing relevance of mitochondrial dysfunction to neurodegeneration, new therapies designed to maintain mitochondrial function could prove beneficial. Photobiomodulation is an alternative therapy proven effective in the treatment of chronic inflammation and neurodegeneration. Previous data demonstrated that 670nm near-infrared (NIR) light-emitting diode (LED) is effective in the amelioration of the disease in a mouse model of MS. Furthermore, experiments suggested an important role for anti-inflammatory cytokines, particularly Interleukin-10 (IL-10), and maintenance of mitochondrial function as important mechanisms mediating disease amelioration. The current studies sought to characterize the immune cell population induced by photobiomodulation which is responsible for the clinical effect noted. With a deeper understanding of the mechanism of protection against disease, the 670nm light would be a promising adjunct therapy for the treatment of MS.