Anti-MOG IgG (Blood)

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Auckland Te Toka Tumai

Test Guide

Anti-MOG IgG (Blood)

Testing Laboratory

Auckland Te Toka Tumai | Auckland Hospital

Department

Immunology

Delphic Registration Code (Alpha Code)

MOG

Test Code (Numeric Code)

8533

Laboratory Handling

Phlebotomy

Serum

Transport

Ambient (8 - 24 °C) within 48 hours; Chilled (4 - 8 °C) if longer than 48 hours

Registration

MOG

Test Adds Requirement

All requests must have either consultant Neurologist or Ophthalmologist approval and be documented to that effect on the request form. Alternatively, the on-line request form may be used.

Sample Stability

Up to 48 hours: 8 - 24 °C; Up to 14 days: 4 - 8 °C; Up to 6 months: -30 °C; Indefinite at - 80 °C

Synonyms

Myelin Oligodendrocyte Glycoprotein antibodies
MOG-IgG

Turnaround Time

2 weeks

This test may be vetted by the laboratory. Please include relevant clinical information on the request form to ensure appropriate tests are approved. See the 'Clinical Information' section below for more information on the indications for testing.

Specimen Type

Serum

Specimen Requirements

Tube/Container Type:

Preferred

SST II (Gold Cap)

Acceptable

Plain (Red Top)

Preferred Sample Volume (ml)

3.5

Minimum Sample Volume (ml)

Paediatric Specimen Requirements

Tube/Container Type:

Preferred

SST II (Gold Cap)

Acceptable

Plain(Microtainer)
SST(Microtainer)

Minimum Sample Volume (ml)

Pre-testing Requirements

All requests must have either consultant Neurologist or Ophthalmologist approval and be documented to that effect on the request form. Alternatively, the on-line request form may be used.

Additional Specimen Information

Paediatric Specimen: 2 mL clotted blood or 1 mL serum

Diagnostic Use

Myelin oligodendrocyte glycoprotein (MOG) is a 28kDa [245 AA] protein expressed exclusively in the CNS on both the outer layer of myelin sheaths and the plasma membranes of oligodendrocytes, with the gene located on chromosome 6 of the HLA locus. MOG belongs to the Ig superfamily, with a single extracellular immunoglobulin variable (Ig V) domain, one transmembrane domain, one cytoplasmic loop and a cytoplasmic tail. Fifteen different alternatively spliced isoforms have been detected in humans. MOG expression commences at the start of nerve myelination and therefore likely plays a role in nerve myelination as well as oligodendrocyte differentiation and maturation. The cytoplasmic tail of MOG determines the intracellular localisation of the various isoforms and as such, it has been proposed that MOG may have a role in intracellular signalling. Furthermore, mouse experimental models showed that cross-linking antibodies to the extracellular component initiated intracellular signalling cascades that resulted in survival signals, changes in cytoskeletal stability and changes in stress responses [1].

Based upon results from ELISA and multiplex assays which used linearized and / or denatured MOG peptides as antigens antibodies to MOG were associated with multiple sclerosis (MS). However, when cell-based assays using the full length conformationally intact MOG protein became available, a number of recent publications have demonstrated relationships between MOG antibodies and optic neuritis (ON) [mostly recurrent], myelitis, brainstem encephalitis as well as acute disseminated encephalomyelitis (ADEM) – like presentations as opposed to classical MS [2-7]. Recent evidence has indicated that (a) MOG IgG is pathogenic (b) patients with MOG IgG have discrete neuro-histopathological features (c) virtually all MOG IgG positive patients are seronegative for AQP4 IgG and (d) cohort studies have identified different clinical presentations, treatment response and prognosis for patients who are MOG IgG positive. It is this evidence that underpins MOG IgG as a disease entity in its own right distinct from MS and AQP4 IgG positive NMOSD patients. This disease entity is now referred to as MOG IgG associated encephalomyelitis (MOG-EM) [8].

Although MS and MOG-EM are differentiated as distinct disease entities they do share a phenotypic (clinical and radiological) overlap during the course of the diseases. This overlap has led to a number of now recognised MOG-EM cases being previously mis-diagnosed as MS. Due to the differences in immunopathogenesis; drugs approved for MS may be either ineffectual and / or harmful in cases of MOG-EM [3-4, 9]. MOG IgG positive patients are typically responsive to immunosuppression and antibody depleting treatments for acute attacks [10-12]. In addition, MOG-EM patients are associated with a high rate of flare-up after cessation of steroids from acute attacks and, as such, require close monitoring and careful steroid tapering [13].

Interpretation

The following Table summarises demographic, clinical presentation, radiologic and laboratory findings in adults with MS, NMO or MOG IgG antibodies who have CNS demyelination [14]

MOG IgG positive CNS demyelination	NMO	MS
Demographics
Women	63-74%	Approx. 90%	70-75%
Median age at onset (years)	31-37	35-45	20-30
Clinical presentation at onset
ON	60-74%	Approx. 45%	15-20%
Bilateral ON (of all ON)	35-41%	8-14%	0-1%
Myelitis	18-23%	Approx. 47%	Rare
Brain stem encephalitis	8-14%	Approx. 3%	Rare
Co-existing autoimmune disease	Rare	Frequent	Rare
MRI
Supratentorial lesions at onset	Approx. 35%	Approx. 50%	>90%
Spinal lesions	Two thirds LETM one third short length central or lateral location	Approx. 94% LETM central location	Short length lateral location
Laboratory findings
Serum	AQP4 IgG Negative MOG IgG POSITIVE	AQP4 IgG POSITIVE MOG IgG Negative	AQP4 IgG Negative MOG IgG POSITIVE
CSF	Oligoclonal banding 6-13% Measles/Rubella/VZV 1-2%	Oligoclonal banding Approx. 28% Measles/Rubella/VZV 1-2%	Oligoclonal banding Approx. 80% Measles/Rubella/VZV 78%

ADEM is characterised by a brief but widespread demyelination in the brain and spinal column. It can be mis-diagnosed as the first attack of MS since symptoms and brain white matter damage on imaging are similar. However, the following features differentiate it from MS:

1. Rapid onset of fever
2. History of recent infection or immunisation
3. Impairment of consciousness (coma in some cases)

Children, (usually <10 years of age) are more likely to have ADEM than adults and MS is rare in children. In addition, ADEM usually consists of a single episode / attack of widespread myelin damage whereas MS features may attacks over time. Location of old lesions by MRI points towards MS as opposed to ADEM since MS can cause brain lesions before symptoms become obvious [15]. Typically ADEM in the paediatric population follows a monophasic course with an overall favourable long-term prognosis with early intervention by way of steroid treatment and / or plasmapheresis. Up to 40% of paediatric patients with inflammatory demyelinating diseases of the CNS are seropositive for MOG antibodies at the disease onset. In the monophasic disease setting, resolution of symptoms correlated with disappearance of MOG antibody. Persistent MOG autoantibodies are rare but have been reported in multiphasic ADEM and they appear to be associated with active progressive disease [16-17].

World-wide, there has been increasingly widespread testing of unselected populations for MOG antibodies which, even in assays that have very good performance characteristics will ultimately undermine their NPV’s and PPV’s which will lead to false positive reporting. In response to this, a group of authors recently published the following criteria for a diagnosis of MOG-EM (all to be met):

1. Monophasic or relapsing acute ON, myelitis, brainstem encephalitis, or encephalitis or, any in combination.
2. MRI findings compatible with CNS demyelination
3. Seropositive MOG IgG as detected by a cell-based assay employing full – length human MOG as the target antigen.

The same authors additionally defined a group of ‘red flags’ to challenge the authenticity of a positive MOG antibody test as defined in the following Table [18]

Disease course

Chronic progressive disease
Sudden onset of symptoms (<4 h from onset to maximum)
Continuous worsening of symptoms over weeks

MRI

Lesion that is adjacent to a lateral ventricle that is ovoid/round or associated with a temporal lobe lesion
Active brain MRI over time with silent increase in lesion burden between relapses

CSF

Bi or Triphasic Measles, Rubella, VZV

Serology

MOG IgG at or just barely above the assay specific cut-off, especially, but not exclusively, if the clinical picture is atypical
MOG IgG detected in CSF but not serum (MOG IgG is typically produced extrathecally)
Double positive AQP4 and MOG IgG. This is very rare and should prompt re-testing for both antibodies

Others

Clinical or paraclinical findings suggesting diagnoses other than MOG-EM, NMOSD or MS
Combined central and peripheral demyelination (MOG is not expressed in the peripheral nervous system)

Reference Intervals

Units: Titres

Age Range	Either Sex
All	< 10

Test Method

Indirect Immunofluorescence assay (IFA) - automated
Manual processing and manual LED microscopy visual evaluation

Limitations / Interference

Grossly haemolysed and/or high lipaemic serum specimens.

Uncertainty of Measurement

Not applicable to this assay

References

1. Peschl P, Bradl M, Hoftberger R, Beyer T, Reindl M. Myelin Oligodendrocyte Glycoprotein: Deciphering a target in demyelinating diseases. Front Imm (2017) 8 https://doi.org/10.3389/fimm2017.00529
2. Jarius S, Ruprecht K, Kleiter I et al. MOG IgG in NMO and related disorders: a multicentre study of 50 patients. Part 1: Frequency, syndrome specificity, influence of disease activity, long term course, association with AQP4-IgG and origin. Neuroinflammation (2016) 13:279
3. Jarius S, Ruprecht K, Kleiter I et al. MOG IgG in NMO and related disorders: a multicentre study of 50 patients. Part 2: Epidemiology, clinical presentation, radiological and laboratory features, treatment responses and long-term outcome. Neuroinflammation (2016) 13:280
4. Jarius S, Ruprecht K, Kleiter I et al. MOG IgG in NMO and related disorders: a multicentre study of 50 patients. Part 3: Brainstem involvement ; frequency, progression and outcome. Neuroinflammation (2016) 13:281
5. Jarius S, Ruprecht K, Kleiter I et al. MOG IgG in NMO and related disorders: a multicentre study of 50 patients. Part 4: Afferent visual system damage after optic neuritis in MOG IgG seropositive versus AQP4 IgG seropositive patients. Neuroinflammation (2016) 13:282
6. Sato DK, Callegaro D, Lana-Peixoto MA et al. Distinction between MOG antibody positive and AQP4 antibody positive NMO spectrum disorders. Neurology (2014) 82: 474-481
7. Ramanathan S, Dale RC, Brilot F. Anti-MOG antibody: The history, clinical phenotype and pathogenicity of a serum biomarker for demyelination. Autoimm Rev (2016) 15: 307-324
8. Reindl M, Jarius S, Rostasy K, Berger T. Myelin oligodendrocyte glycoprotein antibodies: How clinically useful are they? Curr Opin Neurol (2017) 30: 295-301
9. Wildermann B, Jarius S, Schwarz A et al. Failure of alemtuzumab therapy to control MOG encephalomyelitis. Neurology (2017) 89: 207-209
10. Spadaro M, Gerdes LA, Mayer MC et al. Histopathology and clinical course of MOG-antibody-associated-encephalomyelitis. Ann Clin Trans Neurol (2015) 2: 295-301
11. Haochen Y, Wong YY, Lechner C et al. Disease course and treatment responses in children with relapsing myelin oligodendrocyte glycoprotein disease. JAMA Neurol (2018) https://doi.org/10.001/jamaneurol.2017.4601
12. Montcquet A, Collongues N, Papeix C et al. Effectiveness of mycophenolate mofetil as first line therapy in AQP4 IgG, MOG IgG and seronegative neuromyelitis optica spectrum disorders. Mult Scler (2017) 23: 1377-1384
13. Chalmoukou K, Alexopoulos H, Akrivou S, Stathopoulos P, Reindl M, Dalakas MC. Anti-MOG antibodies are frequently associated with steroid sensitive recurrent optic neuritis. Neurol Neuroimmunol Neuroinflamm (2015) :2: 131
14. Weber MS, Derfuss T, Metz I, Bruck W. Defining distinct features of anti-MOG antibody associated central nervous system demyelination. Ther Adv Neurol Disord (2018) 11: 1-15
15. Acute Disseminated Encephalomyelitis Information page. National Institute of Neurological Disorders and Stroke (2018). www.ninds.nih.gov/All-Disorders/Acute-Disseminated-Encephalomyelitis-Information-Page
16. Ketelslegers IA, Van Pelt DE, Bryde S et al. Anti-MOG antibodies plead against MS diagnosis in an acquired demyelinating syndromes cohort. Mult Scler (2015) 21: 1513-1520
17. Probstel AK, Dornmair K, Bittner R et al. Antibodies to MOG are transient in childhood acute disseminated encephalomyelitis. Neurology (2011) 77: 580-588
18. Jarius S, Paul F, Aktas O et al. MOG encephalomyelitis: International recommendations on diagnosis and antibody testing. J Neuroinflamm (2018) 15: 134 - 143

Resources

Last updated: 14/04/2026

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Overview

Testing Laboratory

Department

Delphic Registration Code (Alpha Code)

Test Code (Numeric Code)

Laboratory Handling

Phlebotomy

Transport

Registration

Test Adds Requirement

Sample Stability

Synonyms

Turnaround Time

Specimen

Specimen Type

Specimen Requirements

Tube/Container Type:

Preferred

Acceptable

Preferred Sample Volume (ml)

Minimum Sample Volume (ml)

Paediatric Specimen Requirements

Tube/Container Type:

Preferred

Acceptable

Minimum Sample Volume (ml)

Pre-testing Requirements

Additional Specimen Information

Referral

Aliquot Instructions

Sample Type

Minimum Volume (ml)

Transport to Lab

Clinical Information/Test Method

Diagnostic Use

Interpretation

MOG IgG positive CNS

demyelination

NMO

MS

Demographics

Clinical presentation at onset

MRI

Laboratory findings

Reference Intervals

Test Method

Limitations / Interference

Uncertainty of Measurement

Additional Information

Resources

Contact Information

Contact Information

Enquiry Form

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