DRα1-MOG-35-55 Treatment Reduces Lesion Volumes And Improves Neurological Deficits After Traumatic Brain Injury

Background and purpose Traumatic brain injury(TBI)results in severe neurological impairments without effective treatments.Inflammation participates in the key pathogenic events such as secondary brain injury following TBI,and therefore serves as a promising target for novel therapy.We have recently demonstrated the benefit of the human leukocyte antigen-DRα1 domain linked to MOG-35-55 peptide(DRα1-MOG-35-55)construct to reduce CNS inflammation and tissue injury in animal models of multiple sclerosis and ischemic stroke.The aim of the current study was to determine the impact of DRα1-MOG-35-55 treatment on disease outcome in a mouse model of TBI.Methods TBI was induced in C57BL/6 mice by fluid percussion injury(FPI).Neurodeficits,lesion size,and immune response were determined to examine the therapeutic potential and mechanisms of neuroprotection by DRα1-MOG-35-55 treatment.Results DRα1-MOG-35-55 construct significantly reduced neurodeficits and lesion size after TBI.In DRα1-MOG-35-55-treated TBI mice,reduced infiltration of macrophages and their expression of CD74 and CD86 were seen.In contrast,the expression of CD206 was increased in TBI mice receving DRα1-MOG-35-55.DRα1-MOG-35-55 treatment reduced macrophage infiltration in the brain after TBI.Notably,DRα1-MOG-35-55 reduced the counts of circulating CD11b+cells and their expression of CD74.Conclusion Our results suggest the therapeutic efficacy of the DRα1-MOG-35-55 in a mouse model of TBI.Future advanced studies are required to further determine the therapeutic potential of DRα1-MOG-35-55 construct for TBI treatment.