Presentation is loading. Please wait.

Presentation is loading. Please wait.

Figure 2 Temporal distribution of MOG antibody in serum of 2 relapsing patients with demyelinating diseases Temporal distribution of MOG antibody in serum.

Published byLiese Gertrud Wagner Modified over 6 years ago

Similar presentations

Presentation on theme: "Figure 2 Temporal distribution of MOG antibody in serum of 2 relapsing patients with demyelinating diseases Temporal distribution of MOG antibody in serum."— Presentation transcript:

1 Figure 2 Temporal distribution of MOG antibody in serum of 2 relapsing patients with demyelinating diseases Temporal distribution of MOG antibody in serum of 2 relapsing patients with demyelinating diseases In both patient A (A) and patient B (B), upon treatment mycophenolate mofetil (MMF), myelin oligodendrocyte glycoprotein (MOG) antibody decreased to within the healthy control range (below threshold of positivity), and these low titers were associated with remission. Representative dot plot out of 3 experiments is shown. Magenta lines on graphs represent the positivity threshold (obtained with 24 control samples). Black squares represent serum analysis during acute demyelination episodes, and black circles represent sera during remission. Type of demyelinating episode is shown on graph. (C, D) Representative T2 axial MRI scans demonstrate demyelinating lesions during the first acute event and during convalescence. Patient A (C) had globular deep white matter lesions on acute scan (left panel), which show residual gliosis on convalescent scan and no new lesions (right panel). Patient B (D) had inflammatory lesions in basal ganglia and white matter on acute scan (left panel), with complete resolution on convalescent scan and no new lesions (right panel). Ab = antibody; ADEM = acute disseminated encephalomyelitis; CEREB = cerebellar episode; Ig = immunoglobulin; MFI = mean fluorescence intensity; ON = optic neuritis; TM = transverse myelitis. Russell C. Dale et al. Neurol Neuroimmunol Neuroinflamm 2014;1:e12 © 2014 American Academy of Neurology

Download ppt "Figure 2 Temporal distribution of MOG antibody in serum of 2 relapsing patients with demyelinating diseases Temporal distribution of MOG antibody in serum."

Similar presentations

Figure 2. MRI features of patients with MS who had antibodies to myelin oligodendrocyte glycoprotein MRI features of patients with MS who had antibodies.

Figure 2. MRI features of patients with MS who had antibodies to myelin oligodendrocyte glycoprotein MRI features of patients with MS who had antibodies.
Figure 1. Absence of anti–neurofascin-155 (NF155) antibodies in combined central and peripheral demyelination (CCPD)‏ Absence of anti–neurofascin-155 (NF155)

Figure 1. Absence of anti–neurofascin-155 (NF155) antibodies in combined central and peripheral demyelination (CCPD)‏ Absence of anti–neurofascin-155 (NF155)
Figure 3 Brain MRI findings in patients with MOG-Ab Extensive brain lesions with large diameter (A and B), posterior reversible encephalopathy–like lesions.

Figure 3 Brain MRI findings in patients with MOG-Ab Extensive brain lesions with large diameter (A and B), posterior reversible encephalopathy–like lesions.
Figure 1 Box plot of the venous diameter in lesions

Figure 1 Box plot of the venous diameter in lesions
Figure 4 Neuromyelitis optica spectrum disorder brain lesions

Figure 4 Neuromyelitis optica spectrum disorder brain lesions
Figure 2 GlyR antibody binding

Figure 2 GlyR antibody binding
Figure 2 Association of serum IgG reactivity with MRI measures of disease severity Association of serum IgG reactivity with MRI measures of disease severity.

Figure 2 Association of serum IgG reactivity with MRI measures of disease severity Association of serum IgG reactivity with MRI measures of disease severity.
Figure 2 Orbital MRI findings One-third of myelin oligodendrocyte glycoprotein antibody–positive patients revealed extensive enhancement patterns that.

Figure 2 Orbital MRI findings One-third of myelin oligodendrocyte glycoprotein antibody–positive patients revealed extensive enhancement patterns that.
Figure 3 Antibodies to MOG using different secondary antibodies: Anti-human IgG (H + L), IgG1, or IgM(A) Comparison of binding to full-length myelin oligodendrocyte.

Figure 3 Antibodies to MOG using different secondary antibodies: Anti-human IgG (H + L), IgG1, or IgM(A) Comparison of binding to full-length myelin oligodendrocyte.
Figure 1 Percent positivity by clinical feature Overall, 6

Figure 1 Percent positivity by clinical feature Overall, 6
Figure Brain MRI of the patient throughout the disease course(A) Brain MRI at the time of cerebral toxoplasmosis diagnosis (a) and after 1 month of toxoplasmosis.

Figure Brain MRI of the patient throughout the disease course(A) Brain MRI at the time of cerebral toxoplasmosis diagnosis (a) and after 1 month of toxoplasmosis.
Figure 3 Immune response to neoantigen: Geometric mean titers of antirabies antibody levels over timeAt days 31 and 38, all subjects achieved antibody.

Figure 3 Immune response to neoantigen: Geometric mean titers of antirabies antibody levels over timeAt days 31 and 38, all subjects achieved antibody.
Figure 1 Spine MRI, sagittal and axial views of patients with idiopathic transverse myelitis with VPS37A mutations Spine MRI, sagittal and axial views.

Figure 1 Spine MRI, sagittal and axial views of patients with idiopathic transverse myelitis with VPS37A mutations Spine MRI, sagittal and axial views.
Figure 2 NMDAR-Ab levels, clinical syndromes, and therapy in 8 informative patients with white matter syndromes in association with NMDAR-Ab NMDAR-Ab levels,

Figure 2 NMDAR-Ab levels, clinical syndromes, and therapy in 8 informative patients with white matter syndromes in association with NMDAR-Ab NMDAR-Ab levels,
Figure 3. MRI of compressive optic neuropathy caused by dural lesions in sarcoidosis MRI of compressive optic neuropathy caused by dural lesions in sarcoidosis.

Figure 3. MRI of compressive optic neuropathy caused by dural lesions in sarcoidosis MRI of compressive optic neuropathy caused by dural lesions in sarcoidosis.
Figure Brain MRI and biopsy specimens from the pontine lesion

Figure Brain MRI and biopsy specimens from the pontine lesion
Figure 2 Correlation between total IgG levels and anti-AQP4 IgG titer

Figure 2 Correlation between total IgG levels and anti-AQP4 IgG titer
Figure Chronic inflammatory demyelinating polyneuropathy–like picture in patient with proven Creutzfeldt-Jakob disease (A) Example of partial conduction.

Figure Chronic inflammatory demyelinating polyneuropathy–like picture in patient with proven Creutzfeldt-Jakob disease (A) Example of partial conduction.
Figure MRI and histology of demyelinating lesion(A) Symmetric T2 hyperintensity in the midbrain with relative sparing of cerebral peduncles. MRI and histology.

Figure MRI and histology of demyelinating lesion(A) Symmetric T2 hyperintensity in the midbrain with relative sparing of cerebral peduncles. MRI and histology.
Figure 2 Concordance of results for commercial cell-based assay (CBA) and fluorescence-activated cell sorting (FACS) assays, FACS titers, and disease activity.

Figure 2 Concordance of results for commercial cell-based assay (CBA) and fluorescence-activated cell sorting (FACS) assays, FACS titers, and disease activity.

Similar presentations

Ads by Google