Contributions
Abstract: 208
Type: Scientific Session
Abstract Category: N/A
Introduction: NMOSD is characterized by the presence of aquaporin 4 (AQP4)-specific antibodies in the majority of patients, and by the presence of myelin oligodendrocyte glycoprotein (MOG)-specific antibodies in ~40% of all AQP4-antibody negative patients.
Objectives: In both groups, the pathological changes observed are strikingly similar to those seen in corresponding animal models, suggesting shared mechanisms for lesion formation and localization.
Aims: I will give examples from both NMOSD patients and animal models to reveal the mechanisms responsible for lesion formation and localization.
Methods: Comparative analysis of pathology from human patients and animal models.
Results:
(a) lesions are initiated by activated central nervous System (CNS) antigen-specific T cells which open the blood-brain barrier in the vast majority of cases,
(b) the ratios between pathogenic antibodies and CNS antigen-specific T cells determine whether multifocal small lesions or single large lesions form,
(c) lesion formation and localization is driven by the amount of CNS antigens available for the presentation of antigens, the activation of T cells, and the binding of antibodies,
(d) lesion localization may depend on major histocompatibility complex (MHC) and non-MHC genes, age, gender, and mode of sensitization.
(e) lesions may also derive from the diffusion of antibodies from circumventricular organs, and from the CSF.
Conclusion: several mechanisms cooperate in lesion formation and localization in NMOSD and corresponding animal models.
Disclosure: Monika Bradl: nothing to disclose.
Abstract: 208
Type: Scientific Session
Abstract Category: N/A
Introduction: NMOSD is characterized by the presence of aquaporin 4 (AQP4)-specific antibodies in the majority of patients, and by the presence of myelin oligodendrocyte glycoprotein (MOG)-specific antibodies in ~40% of all AQP4-antibody negative patients.
Objectives: In both groups, the pathological changes observed are strikingly similar to those seen in corresponding animal models, suggesting shared mechanisms for lesion formation and localization.
Aims: I will give examples from both NMOSD patients and animal models to reveal the mechanisms responsible for lesion formation and localization.
Methods: Comparative analysis of pathology from human patients and animal models.
Results:
(a) lesions are initiated by activated central nervous System (CNS) antigen-specific T cells which open the blood-brain barrier in the vast majority of cases,
(b) the ratios between pathogenic antibodies and CNS antigen-specific T cells determine whether multifocal small lesions or single large lesions form,
(c) lesion formation and localization is driven by the amount of CNS antigens available for the presentation of antigens, the activation of T cells, and the binding of antibodies,
(d) lesion localization may depend on major histocompatibility complex (MHC) and non-MHC genes, age, gender, and mode of sensitization.
(e) lesions may also derive from the diffusion of antibodies from circumventricular organs, and from the CSF.
Conclusion: several mechanisms cooperate in lesion formation and localization in NMOSD and corresponding animal models.
Disclosure: Monika Bradl: nothing to disclose.