| Literature DB >> 33002405 |
Dennis Fitzgerald1, Micheline Laurent2, Michael Funaro1,2, Asaff Harel3, Tracey DeAngelis4, Catherine Bangeranye1, Souhel Najjar3, Inna Tabansky2,5, Joel N H Stern1,2,3,6.
Abstract
Auto-reactive T cells are fundamental to many autoimmune processes, including neuromyelitis optica spectrum disorder (NMOSD). Several lines of evidence indicate that an antibody against aquaporin-4 (AQP4) is present in NMOSD patients. Further, this AQP4 antibody is pathogenic and can cause profound neurological damage. T cells are fundamental to many autoimmune processes, including NMOSD. Here we review work from animal models to discuss mechanisms by which auto-reactive T cells modulate the process by which antibodies cross the blood-brain barrier and orchestrate the local inflammatory milieu underlying NMOSD pathophysiology. We also examine clinical studies that document the presence of AQP4-specific T cells and the unique cytokine profile of NMOSD patients. This work encourages a renewed and broadened attention to the fundamental role of T cells in neuroautoimmune conditions which will hopefully lead to new therapies and better patients' outcomes.Entities:
Year: 2020 PMID: 33002405
Source DB: PubMed Journal: Discov Med ISSN: 1539-6509 Impact factor: 2.970