Contributions
Abstract: EP1475
Type: Poster Sessions
Abstract Category: Pathology and pathogenesis of MS - Immunology
Background: Multiple sclerosis (MS) and neuromyelitis optica spectrum disorders (NMOSD) are both autoimmune central nervous system (CNS) disorders. And anti-aquaporin-4 (AQP4) positive patients represents overwhelming majority in NMOSD. Anti-myelin oligodendrocyte glycoprotein (MOG) positive CNS disorder (MOG+CD) involves a case who had both anti-MOG antibody and CNS involvement. These disorders share similar but diverse pathological and clinical characteristics. It is worth noting that T cell and related inflammatory cytokines have been proved to make considerable contributions for these diseases.
Objective: Investigate T cell subsets in peripheral blood monocytes (PBMCs) among MOG+CNS disorders, AQP4+NMOSD and MS, on basis of which, their contribution to the pathogenesis and clinical features of those disorders.
Methods: We enrolled 10 healthy controls (HCs)、20 relapse-remitting MS patients, 20 patients with MOG+CD, 20 patients with AQP4+NMOSD, who were all in remitting phase. Flow cytometry (FCM) was employed to detect T cell subsets (CD3, CD4, CD8, Th1, Th2, Th17, Treg, Th1/Th2, Th17/Treg). Meanwhile, evaluate the otherness of these cell subsets of and their correlation with clinical information.
Results and conclusions: MOG+ CD has equivalent sex and age constituent but less EDSS score (P=0.014) compared with AQP4+NMOSD. Compared with HCs, there is lower level of lymphocyte in AQP4+NMOSD group (P=0.02), similar level of CD3+ T cell, CD4+ T cell, CD8+ T cell,Th1 and Th1/Th2 among MOG+CD group、AQP4+NMOSD group and MS group, relatively lower level of Th2 in AQP4+NMOSD group (P=0.073) and MS group (P=0.053) but the difference is not significant and higher level of Th17 and Th17/Treg in both AQP4+NMOSD (PTh17= 0.003, PTh17/Treg< 0.001) and MS group (PTh17< 0.001,PTh17/Treg< 0.001) but milder these index in MOG+CD group. And in MS group, Th17 could be viewed as disease predictive factor of prognosis. Additionally, the potential contribution of Th2 to relapse in both AQP4+NMOSD and MOG+CD group are also identified and in lower range of Th2, appropriately increasing it could be helpful for prolonging the average attack interval in AQP4+NMOSD group. For Treg, its compensatory increasing effect when relapse is more sufficient in MOG+CD group compared to AQP4+NMOSD group, which resulted in severe neurological function damage (higher EDSS score) even though unfrequently attack recently resulting from steroid application.
Disclosure: Jia Liu: nothing to disclose.
Masahiro Mori: nothing to disclose.
Kazuo Sugimoto: nothing to disclose.
Akiyuki Uzawa : nothing to disclose.
Tomohiko Uchida: nothing to disclose.
Hiroki Masuda: nothing to disclose.
Ryohei Ohtani: nothing to disclose.
Sagiri lsose: nothing to disclose.
Kimihito Arai: nothing to disclose.
Satoshi Kuwabara: serves as an asociate editor of Journal of Neurology, Neurosurgery, and Psychiatry, and an editorual board member of Journal of the Neurological Sciences, and received a grant from Japanese Agency of Medical Research and Development.
Abstract: EP1475
Type: Poster Sessions
Abstract Category: Pathology and pathogenesis of MS - Immunology
Background: Multiple sclerosis (MS) and neuromyelitis optica spectrum disorders (NMOSD) are both autoimmune central nervous system (CNS) disorders. And anti-aquaporin-4 (AQP4) positive patients represents overwhelming majority in NMOSD. Anti-myelin oligodendrocyte glycoprotein (MOG) positive CNS disorder (MOG+CD) involves a case who had both anti-MOG antibody and CNS involvement. These disorders share similar but diverse pathological and clinical characteristics. It is worth noting that T cell and related inflammatory cytokines have been proved to make considerable contributions for these diseases.
Objective: Investigate T cell subsets in peripheral blood monocytes (PBMCs) among MOG+CNS disorders, AQP4+NMOSD and MS, on basis of which, their contribution to the pathogenesis and clinical features of those disorders.
Methods: We enrolled 10 healthy controls (HCs)、20 relapse-remitting MS patients, 20 patients with MOG+CD, 20 patients with AQP4+NMOSD, who were all in remitting phase. Flow cytometry (FCM) was employed to detect T cell subsets (CD3, CD4, CD8, Th1, Th2, Th17, Treg, Th1/Th2, Th17/Treg). Meanwhile, evaluate the otherness of these cell subsets of and their correlation with clinical information.
Results and conclusions: MOG+ CD has equivalent sex and age constituent but less EDSS score (P=0.014) compared with AQP4+NMOSD. Compared with HCs, there is lower level of lymphocyte in AQP4+NMOSD group (P=0.02), similar level of CD3+ T cell, CD4+ T cell, CD8+ T cell,Th1 and Th1/Th2 among MOG+CD group、AQP4+NMOSD group and MS group, relatively lower level of Th2 in AQP4+NMOSD group (P=0.073) and MS group (P=0.053) but the difference is not significant and higher level of Th17 and Th17/Treg in both AQP4+NMOSD (PTh17= 0.003, PTh17/Treg< 0.001) and MS group (PTh17< 0.001,PTh17/Treg< 0.001) but milder these index in MOG+CD group. And in MS group, Th17 could be viewed as disease predictive factor of prognosis. Additionally, the potential contribution of Th2 to relapse in both AQP4+NMOSD and MOG+CD group are also identified and in lower range of Th2, appropriately increasing it could be helpful for prolonging the average attack interval in AQP4+NMOSD group. For Treg, its compensatory increasing effect when relapse is more sufficient in MOG+CD group compared to AQP4+NMOSD group, which resulted in severe neurological function damage (higher EDSS score) even though unfrequently attack recently resulting from steroid application.
Disclosure: Jia Liu: nothing to disclose.
Masahiro Mori: nothing to disclose.
Kazuo Sugimoto: nothing to disclose.
Akiyuki Uzawa : nothing to disclose.
Tomohiko Uchida: nothing to disclose.
Hiroki Masuda: nothing to disclose.
Ryohei Ohtani: nothing to disclose.
Sagiri lsose: nothing to disclose.
Kimihito Arai: nothing to disclose.
Satoshi Kuwabara: serves as an asociate editor of Journal of Neurology, Neurosurgery, and Psychiatry, and an editorual board member of Journal of the Neurological Sciences, and received a grant from Japanese Agency of Medical Research and Development.