Neurology(R) neuroimmunology & neuroinflammation · 2025
MOG IgG3-Subclass Antibodies in MOG-Associated Disease: Insights From a Pediatric Case With IgG1 Deficiency and Literature Review.
СтатьяКлинический случайОбзорНазвание и аннотация: Перевод в очереди
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Fetta Anna, Conti Francesca, Lopalco Agnese, Corsini Chiara, Moratti Mattia, Morelli Luana, Ricciardiello Fortuna, Toni Francesco, Lanari Marcello, Liguori Rocco, Cordelli Duccio Maria, Giannoccaro Maria Pia
Аннотация
OBJECTIVES: This report details a pediatric case of myelin oligodendrocyte glycoprotein antibody disease (MOGAD) characterized by isolated MOG-IgG3 positivity and IgG1 deficiency, highlighting a unique serologic profile and exploring its immunologic significance. In addition, a review of MOGAD cases with isolated MOG-IgG3 antibodies is included.
METHODS: A 12-year-old boy presenting with a progressive neurologic syndrome underwent clinical, radiologic, and laboratory evaluation.
RESULTS: MRI showed extensive brain and spinal lesions. MOG-IgG3 antibodies were identified in serum and CSF by live cell-based assay, while other MOG-IgG subclasses were not detected. Serum IgG1 was low at baseline and throughout follow-up. First-line immunotherapy treatment led to significant improvement, with no relapses at 2-year follow-up.
DISCUSSION: This case highlights the potential role of subclinical IgG1 deficiency in shaping the predominance or selective detection of MOG-IgG3 in MOGAD. While most MOG antibodies are predominantly of the IgG1 isotype, our review identified a few cases with isolated MOG-IgG3 antibodies. A possible contribution to pathogenesis cannot be excluded, and the patient's inability to produce a balanced IgG subclass profile could have favored a sustained IgG3 response. Larger studies are needed to clarify the clinical significance of MOG-IgG3 in MOGAD.
METHODS: A 12-year-old boy presenting with a progressive neurologic syndrome underwent clinical, radiologic, and laboratory evaluation.
RESULTS: MRI showed extensive brain and spinal lesions. MOG-IgG3 antibodies were identified in serum and CSF by live cell-based assay, while other MOG-IgG subclasses were not detected. Serum IgG1 was low at baseline and throughout follow-up. First-line immunotherapy treatment led to significant improvement, with no relapses at 2-year follow-up.
DISCUSSION: This case highlights the potential role of subclinical IgG1 deficiency in shaping the predominance or selective detection of MOG-IgG3 in MOGAD. While most MOG antibodies are predominantly of the IgG1 isotype, our review identified a few cases with isolated MOG-IgG3 antibodies. A possible contribution to pathogenesis cannot be excluded, and the patient's inability to produce a balanced IgG subclass profile could have favored a sustained IgG3 response. Larger studies are needed to clarify the clinical significance of MOG-IgG3 in MOGAD.