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Anti-MOG antibodies are present in a subgroup of patients with a neuromyelitis optica phenotype.

Pröbstel AK, Rudolf G, Dornmair K, Collongues N, Chanson JB, Sanderson NS, Lindberg RL, Kappos L, de Seze J, Derfuss T - J Neuroinflammation (2015)

Bottom Line: Anti-MOG antibodies were found in 4/17 patients with AQP4-seronegative NMO/NMOSD, but in none of the AQP4-seropositive NMO/NMOSD (n = 31) or RR-MS patients (n = 48).MOG-seropositive patients show a diverse clinical phenotype with clinical features resembling both NMO (attacks mainly confined to the spinal cord and optic nerves) and MS with an opticospinal presentation (positive OCBs, brain lesions).Anti-MOG antibodies can serve as a diagnostic and maybe prognostic tool in patients with an AQP4-seronegative NMO phenotype and should be tested in those patients.

View Article: PubMed Central - PubMed

Affiliation: Department of Neurology, University Hospital Basel, Petersgraben 4, 4031, Basel, Switzerland. anne-katrin.proebstel@usb.ch.

ABSTRACT

Background: Antibodies against myelin oligodendrocyte glycoprotein (MOG) have been identified in a subgroup of pediatric patients with inflammatory demyelinating disease of the central nervous system (CNS) and in some patients with neuromyelitis optica spectrum disorder (NMOSD). The aim of this study was to examine the frequency, clinical features, and long-term disease course of patients with anti-MOG antibodies in a European cohort of NMO/NMOSD.

Findings: Sera from 48 patients with NMO/NMOSD and 48 patients with relapsing-remitting multiple sclerosis (RR-MS) were tested for anti-aquaporin-4 (AQP4) and anti-MOG antibodies with a cell-based assay. Anti-MOG antibodies were found in 4/17 patients with AQP4-seronegative NMO/NMOSD, but in none of the AQP4-seropositive NMO/NMOSD (n = 31) or RR-MS patients (n = 48). MOG-seropositive patients tended towards younger disease onset with a higher percentage of patients with pediatric (<18 years) disease onset (MOG+, AQP4+, MOG-/AQP4-: 2/4, 3/31, 0/13). MOG-seropositive patients presented more often with positive oligoclonal bands (OCBs) (3/3, 5/29, 1/13) and brain magnetic resonance imaging (MRI) lesions during disease course (2/4, 5/31, 1/13). Notably, the mean time to the second attack affecting a different CNS region was longer in the anti-MOG antibody-positive group (11.3, 3.2, 3.4 years).

Conclusions: MOG-seropositive patients show a diverse clinical phenotype with clinical features resembling both NMO (attacks mainly confined to the spinal cord and optic nerves) and MS with an opticospinal presentation (positive OCBs, brain lesions). Anti-MOG antibodies can serve as a diagnostic and maybe prognostic tool in patients with an AQP4-seronegative NMO phenotype and should be tested in those patients.

No MeSH data available.


Related in: MedlinePlus

Overview of patient cohort, antibody status, and anti-MOG antibody levels. (A) Patient cohort and antibody status: The study comprised a total of 135 participants including patients with NMO/NMOSD (n = 48), relapsing-remitting multiple sclerosis (RR-MS) (n = 48), and healthy donors (n = 39). Of the NMO/NMOSD patients, 31 were positive for anti-AQP4 antibodies (AQP4+) with the cell-based assay (CBA) while only 22 patients tested positive with indirect immunofluorescence (iIF). All of the AQP4-seropositive patients were negative for anti-MOG antibodies (MOG−). Of the AQP4-seronegative patients (AQP4−), four patients had anti-MOG antibodies (MOG+) (CBA), while 13 patients had no detectable antibodies against either AQP4 or MOG. (B) Anti-MOG antibody levels: Anti-MOG reactivity was analyzed with the CBA and is expressed as the geometric mean channel fluorescence (GMCF) ratio of the MOG-transfected cell line divided by the empty vector-transfected cell line. Values shown represent the (mean) GMCF ratio of one to four experiments. The cutoff used (dotted line) is the mean GMCF ratio of the healthy donor group measured in parallel (n = 39) plus two standard deviations (cutoff = 1.45). Using this cutoff, 4 of the 17 (23.5%) NMO/NMOSD sera were positive for anti-MOG antibodies (empty red squares), all of which were AQP4-seronegative (filled red squares). None of the AQP4-seropositive NMO/NMOSD patients (filled red circles) and none of the RR-MS patients (filled light red triangles) were positive for anti-MOG antibodies.
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Fig1: Overview of patient cohort, antibody status, and anti-MOG antibody levels. (A) Patient cohort and antibody status: The study comprised a total of 135 participants including patients with NMO/NMOSD (n = 48), relapsing-remitting multiple sclerosis (RR-MS) (n = 48), and healthy donors (n = 39). Of the NMO/NMOSD patients, 31 were positive for anti-AQP4 antibodies (AQP4+) with the cell-based assay (CBA) while only 22 patients tested positive with indirect immunofluorescence (iIF). All of the AQP4-seropositive patients were negative for anti-MOG antibodies (MOG−). Of the AQP4-seronegative patients (AQP4−), four patients had anti-MOG antibodies (MOG+) (CBA), while 13 patients had no detectable antibodies against either AQP4 or MOG. (B) Anti-MOG antibody levels: Anti-MOG reactivity was analyzed with the CBA and is expressed as the geometric mean channel fluorescence (GMCF) ratio of the MOG-transfected cell line divided by the empty vector-transfected cell line. Values shown represent the (mean) GMCF ratio of one to four experiments. The cutoff used (dotted line) is the mean GMCF ratio of the healthy donor group measured in parallel (n = 39) plus two standard deviations (cutoff = 1.45). Using this cutoff, 4 of the 17 (23.5%) NMO/NMOSD sera were positive for anti-MOG antibodies (empty red squares), all of which were AQP4-seronegative (filled red squares). None of the AQP4-seropositive NMO/NMOSD patients (filled red circles) and none of the RR-MS patients (filled light red triangles) were positive for anti-MOG antibodies.

Mentions: In total, 48 patients with NMO/NMOSD were included in the study: 4 of the 48 patients tested positive for anti-MOG antibodies, all of which were negative for anti-AQP4-antibodies (Figure 1). Tested with the iIF assay, 22 patients were positive for anti-AQP4-antibodies, while testing with the CBA revealed that 31 patients were anti-AQP4 antibody-positive (Figure 1A). Only one patient was tested positive with the iIF assay, but negative with the CBA. The remaining 13 patients were seronegative for both antibodies tested (Figure 1).Figure 1


Anti-MOG antibodies are present in a subgroup of patients with a neuromyelitis optica phenotype.

Pröbstel AK, Rudolf G, Dornmair K, Collongues N, Chanson JB, Sanderson NS, Lindberg RL, Kappos L, de Seze J, Derfuss T - J Neuroinflammation (2015)

Overview of patient cohort, antibody status, and anti-MOG antibody levels. (A) Patient cohort and antibody status: The study comprised a total of 135 participants including patients with NMO/NMOSD (n = 48), relapsing-remitting multiple sclerosis (RR-MS) (n = 48), and healthy donors (n = 39). Of the NMO/NMOSD patients, 31 were positive for anti-AQP4 antibodies (AQP4+) with the cell-based assay (CBA) while only 22 patients tested positive with indirect immunofluorescence (iIF). All of the AQP4-seropositive patients were negative for anti-MOG antibodies (MOG−). Of the AQP4-seronegative patients (AQP4−), four patients had anti-MOG antibodies (MOG+) (CBA), while 13 patients had no detectable antibodies against either AQP4 or MOG. (B) Anti-MOG antibody levels: Anti-MOG reactivity was analyzed with the CBA and is expressed as the geometric mean channel fluorescence (GMCF) ratio of the MOG-transfected cell line divided by the empty vector-transfected cell line. Values shown represent the (mean) GMCF ratio of one to four experiments. The cutoff used (dotted line) is the mean GMCF ratio of the healthy donor group measured in parallel (n = 39) plus two standard deviations (cutoff = 1.45). Using this cutoff, 4 of the 17 (23.5%) NMO/NMOSD sera were positive for anti-MOG antibodies (empty red squares), all of which were AQP4-seronegative (filled red squares). None of the AQP4-seropositive NMO/NMOSD patients (filled red circles) and none of the RR-MS patients (filled light red triangles) were positive for anti-MOG antibodies.
© Copyright Policy - open-access
Related In: Results  -  Collection

License 1 - License 2
Show All Figures
getmorefigures.php?uid=PMC4359547&req=5

Fig1: Overview of patient cohort, antibody status, and anti-MOG antibody levels. (A) Patient cohort and antibody status: The study comprised a total of 135 participants including patients with NMO/NMOSD (n = 48), relapsing-remitting multiple sclerosis (RR-MS) (n = 48), and healthy donors (n = 39). Of the NMO/NMOSD patients, 31 were positive for anti-AQP4 antibodies (AQP4+) with the cell-based assay (CBA) while only 22 patients tested positive with indirect immunofluorescence (iIF). All of the AQP4-seropositive patients were negative for anti-MOG antibodies (MOG−). Of the AQP4-seronegative patients (AQP4−), four patients had anti-MOG antibodies (MOG+) (CBA), while 13 patients had no detectable antibodies against either AQP4 or MOG. (B) Anti-MOG antibody levels: Anti-MOG reactivity was analyzed with the CBA and is expressed as the geometric mean channel fluorescence (GMCF) ratio of the MOG-transfected cell line divided by the empty vector-transfected cell line. Values shown represent the (mean) GMCF ratio of one to four experiments. The cutoff used (dotted line) is the mean GMCF ratio of the healthy donor group measured in parallel (n = 39) plus two standard deviations (cutoff = 1.45). Using this cutoff, 4 of the 17 (23.5%) NMO/NMOSD sera were positive for anti-MOG antibodies (empty red squares), all of which were AQP4-seronegative (filled red squares). None of the AQP4-seropositive NMO/NMOSD patients (filled red circles) and none of the RR-MS patients (filled light red triangles) were positive for anti-MOG antibodies.
Mentions: In total, 48 patients with NMO/NMOSD were included in the study: 4 of the 48 patients tested positive for anti-MOG antibodies, all of which were negative for anti-AQP4-antibodies (Figure 1). Tested with the iIF assay, 22 patients were positive for anti-AQP4-antibodies, while testing with the CBA revealed that 31 patients were anti-AQP4 antibody-positive (Figure 1A). Only one patient was tested positive with the iIF assay, but negative with the CBA. The remaining 13 patients were seronegative for both antibodies tested (Figure 1).Figure 1

Bottom Line: Anti-MOG antibodies were found in 4/17 patients with AQP4-seronegative NMO/NMOSD, but in none of the AQP4-seropositive NMO/NMOSD (n = 31) or RR-MS patients (n = 48).MOG-seropositive patients show a diverse clinical phenotype with clinical features resembling both NMO (attacks mainly confined to the spinal cord and optic nerves) and MS with an opticospinal presentation (positive OCBs, brain lesions).Anti-MOG antibodies can serve as a diagnostic and maybe prognostic tool in patients with an AQP4-seronegative NMO phenotype and should be tested in those patients.

View Article: PubMed Central - PubMed

Affiliation: Department of Neurology, University Hospital Basel, Petersgraben 4, 4031, Basel, Switzerland. anne-katrin.proebstel@usb.ch.

ABSTRACT

Background: Antibodies against myelin oligodendrocyte glycoprotein (MOG) have been identified in a subgroup of pediatric patients with inflammatory demyelinating disease of the central nervous system (CNS) and in some patients with neuromyelitis optica spectrum disorder (NMOSD). The aim of this study was to examine the frequency, clinical features, and long-term disease course of patients with anti-MOG antibodies in a European cohort of NMO/NMOSD.

Findings: Sera from 48 patients with NMO/NMOSD and 48 patients with relapsing-remitting multiple sclerosis (RR-MS) were tested for anti-aquaporin-4 (AQP4) and anti-MOG antibodies with a cell-based assay. Anti-MOG antibodies were found in 4/17 patients with AQP4-seronegative NMO/NMOSD, but in none of the AQP4-seropositive NMO/NMOSD (n = 31) or RR-MS patients (n = 48). MOG-seropositive patients tended towards younger disease onset with a higher percentage of patients with pediatric (<18 years) disease onset (MOG+, AQP4+, MOG-/AQP4-: 2/4, 3/31, 0/13). MOG-seropositive patients presented more often with positive oligoclonal bands (OCBs) (3/3, 5/29, 1/13) and brain magnetic resonance imaging (MRI) lesions during disease course (2/4, 5/31, 1/13). Notably, the mean time to the second attack affecting a different CNS region was longer in the anti-MOG antibody-positive group (11.3, 3.2, 3.4 years).

Conclusions: MOG-seropositive patients show a diverse clinical phenotype with clinical features resembling both NMO (attacks mainly confined to the spinal cord and optic nerves) and MS with an opticospinal presentation (positive OCBs, brain lesions). Anti-MOG antibodies can serve as a diagnostic and maybe prognostic tool in patients with an AQP4-seronegative NMO phenotype and should be tested in those patients.

No MeSH data available.


Related in: MedlinePlus