Abstract
Neuromyelitis optica spectrum disorder (NMOSD) likely results from humoral immune abnormalities. The role that helper T cells play in the pathogenesis of this disease is not fully understood. To ascertain the clinical significance of two important costimulatory molecules required for T-cell activation in the peripheral blood of patients with NMOSD, we examined the expression levels of a membrane- and soluble-type inducible costimulatory molecule (ICOS), its ligand (ICOSL), programmed death-1 (PD-1), and its ligand (PD-L1) in the peripheral blood of 30 patients with NMOSD and compared these levels with those in patients with longitudinally extensive transverse myelitis (LETM), those with optic neuritis (ON), and healthy controls (HCs). Our results showed that the ICOS/ICOSL and PD-1/PD-L1 pathways may play important roles in the early stages of NMOSD pathogenesis. ICOS and PD-1 are potential therapeutic targets and valuable biomarkers for the differential diagnosis of early-stage NMOSD.
Highlights
Neuromyelitis optica spectrum disorder (NMOSD) likely results from humoral immune abnormalities
With the discovery of AQP-4 IgG, the consensus regarding the pathogenesis of NMOSD has shifted from a strictly autoimmune condition to a central nervous system (CNS) demyelination disease mediated primarily by humoral immunity
In-depth research on the pathogenic mechanisms has determined that AQP-4 IgG cannot fully explain the pathological process of NMOSD, primarily with regard to the following aspects: (1) AQP4-IgG infused into the peripheral blood of mice does not completely pass the blood-brain barrier and cannot cause disease in mice; following the destruction of the blood-brain barrier in experimental mice using the pertussis virus and lipopolysaccharide, infused AQP-4 IgG did not reproduce the disease condition
Summary
Neuromyelitis optica spectrum disorder (NMOSD) likely results from humoral immune abnormalities. PD-L1, known as B7-H1, produces an inhibitory signal after binding to its receptor, inducing T cell apoptosis and inhibiting T cell activation and proliferation[5,9], thereby negatively regulating the immune response and participating in the regulation of immune tolerance, responses to microbial infection, and tumor immune evasion[10,11] In addition to their roles in immuno-oncology mechanisms, which have received broad attention, the roles of these costimulatory molecules in autoimmune diseases and the application of related monoclonal antibodies in the treatment of these diseases have increasingly become a hot research topic. Exploring their possible roles and mechanisms in NMOSD immunopathology is important for elucidating the pathological mechanism of this disease, its qualitative and timely diagnosis, and searching for new targets for therapeutic intervention
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