Biological characteristics of transcription factor RelB in different immune cell types: implications for the treatment of multiple sclerosis.

Transcription factor RelB is a member of the nuclear factror-kappa B (NF-κB) family, which plays a crucial role in mediating immune responses. Plenty of studies have demonstrated that RelB actively contributes to lymphoid organ development, dendritic cells maturation and function and T cells differentiation, as well as B cell development and survival. RelB deficiency may cause a variety of immunological disorders in both mice and humans. Multiple sclerosis (MS) is an inflammatory and demyelinating disease of the central nervous system which involves a board of immune cell populations. Thereby, RelB may exert an impact on MS by modulating the functions of dendritic cells and the differentiation of T cells and B cells. Despite intensive research, the role of RelB in MS and its animal model, experimental autoimmune encephalomyelitis, is still unclear. Herein, we give an overview of the biological characters of RelB, summarize the updated knowledge regarding the role of RelB in different cell types that contribute to MS pathogenesis and discuss the potential RelB-targeted therapeutic implications for MS.

The GTF2I rs117026326 polymorphism is associated with neuromyelitis optica spectrum disorder but not with multiple sclerosis in a Northern Han Chinese population.

Multiple sclerosis (MS) and neuromyelitis optica spectrum disorder (NMOSD) are common demyelinating disorders of the central nervous system. The etiology and pathogenesis of MS and NMOSD remain unclear. The pathogenesis of these two diseases involves a genetic predisposition as well as environmental factors. NMOSD sometimes co-exists with Sjögren's syndrome, systemic lupus erythematosus (SLE), and rheumatoid arthritis (RA), and these diseases are frequently associated with central nervous system disorder involvement, as manifest in MS- and NMOSD-like clinical features. Genetic variant rs117026326 upstream of the general transcription factor II-I (GTF2I) has been associated with primary Sjögren's syndrome, SLE and RA in East Asian populations. In this study, we genotyped single nucleotide rs117026326 polymorphisms of the GTF2I gene in 168 patients with MS, 144 patients with NMOSD, and 1403 healthy controls. We observed a significant genetic association between the variant rs117026326 and NMOSD (P = 1.09 × 10-11, OR = 2.535), however, the association with MS was not significant (P = .4289, OR = 1.129). Gene expression analyses showed that there was no significant association between the messenger RNA expression of GTF2I and genotypes at the variant. We conclude that the risk T allele of rs117026326 increases the risk of NMOSD, suggesting that NMOSD and MS may have different genetic risk factors.

A case report: Non-alcoholic Wernicke encephalopathy associated with polyneuropathy.

We report a rare case of non-alcoholic Wernicke encephalopathy (WE) with polyneuropathy. A 24-year-old woman who had recently served a 4-month prison sentence and underwent a short period of dieting manifested slow response, weakness, language disorder and amnesia. Brain magnetic resonance imaging (MRI) revealed typical lesions of WE. Examination of nerve conduction velocity revealed sensory-motor axonal polyneuropathy. The patient was immediately treated with thiamine. Neurological symptoms were alleviated in a few days and abnormal signals were markedly decreased in a follow-up MRI 1 week later. Polyneuropathy symptoms ameliorated during hospital therapy and significantly improved after 4 months. This case suggests that WE may be associated with polyneuropathy in non-alcoholic patients. Early thiamine treatment in symptomatic patients may improve prognosis.