| WB | 1/500-1/1000 | Human,Mouse,Rat |
| IF | 咨询技术 | Human,Mouse,Rat |
| IHC | 1/50-1/100 | Human,Mouse,Rat |
| ICC | 1/50-1/200 | Human,Mouse,Rat |
| FCM | 咨询技术 | Human,Mouse,Rat |
| Elisa | 咨询技术 | Human,Mouse,Rat |
| Aliases | BTN6; BTNL11; MOGIG2; NRCLP7 |
| Entrez GeneID | 4340 |
| WB Predicted band size | Calculated MW: 28 kDa; Observed MW: 28 kDa |
| Host/Isotype | Rabbit IgG |
| Antibody Type | Primary antibody |
| Storage | Store at 4°C short term. Aliquot and store at -20°C long term. Avoid freeze/thaw cycles. |
| Species Reactivity | Human,Mouse,Rat |
| Immunogen | A synthesized peptide derived from human Myelin oligodendrocyte glycoprotein |
| Formulation | Purified antibody in PBS with 0.05% sodium azide. |
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以下是3-4条关于MOG抗体(髓鞘少突胶质细胞糖蛋白抗体)的参考文献及其摘要概括：
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1. **文献名称**：*MOG antibody-associated disease: a review of its clinical spectrum, pathophysiology, and treatment*
**作者**：Pröbstel AK, et al.
**摘要**：该综述总结了MOG抗体相关疾病(MOGAD)的临床特征，包括视神经炎、横贯性脊髓炎和脑炎等表现。文章讨论了MOG抗体的致病机制、与其他脱髓鞘疾病(如AQP4抗体阳性的NMOSD)的差异，并强调免疫治疗(如类固醇和免疫抑制剂)的疗效及复发管理策略。
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2. **文献名称**：*Clinical and therapeutic implications of MOG-IgG detection in demyelinating diseases*
**作者**：Jarius S, Wildemann B.
**摘要**：研究分析了MOG抗体在不同脱髓鞘疾病中的诊断价值，指出MOG抗体阳性患者可能具有独特的临床特征(如儿童患者比例较高、视神经炎更易复发但预后较好)。文章建议将MOG抗体检测纳入脱髓鞘疾病的常规诊断流程，以优化治疗选择。
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3. **文献名称**：*Distinct clinical and imaging features of MOG-IgG-positive and AQP4-IgG-positive neuromyelitis optica spectrum disorders*
**作者**：Sato DK, et al.
**摘要**：通过比较MOG抗体阳性与AQP4抗体阳性的NMOSD患者，发现MOG抗体阳性患者更易出现双侧视神经炎、脊髓病变范围较小，且对类固醇治疗反应更佳。影像学显示MOGAD患者脑部病变较少，但可能累及视神经鞘膜。
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4. **文献名称**：*MOG-IgG in pediatric patients: clinical characteristics and proposed diagnostic criteria*
**作者**：Hacohen Y, et al.
**摘要**：针对儿童MOG抗体相关疾病的研究，提出儿童患者常表现为急性播散性脑脊髓炎(ADEM)或复发性视神经炎，且MOG抗体滴度与疾病活动性相关。作者建议将抗体检测与临床特征结合，制定儿童MOGAD的诊断标准。
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以上文献涵盖了MOG抗体疾病的临床特点、诊断分型及治疗方向，可作为该领域的重要参考。
Myelin oligodendrocyte glycoprotein (MOG) is a protein located on the surface of myelin sheaths in the central nervous system (CNS). Antibodies targeting MOG (MOG-IgG) are associated with a spectrum of autoimmune demyelinating disorders, now recognized as a distinct clinical entity termed MOG antibody-associated disease (MOGAD). Unlike multiple sclerosis (MS) or aquaporin-4 (AQP4)-positive neuromyelitis optica spectrum disorder (NMOSD), MOGAD has unique clinical and pathological features. MOG-IgG is detected using cell-based assays, which improved diagnostic accuracy compared to older techniques.
MOGAD commonly presents with optic neuritis, transverse myelitis, or acute disseminated encephalomyelitis (ADEM)-like episodes, often with relapses. Unlike AQP4-positive NMOSD, it affects both adults and children, with pediatric cases frequently showing ADEM phenotypes. MRI findings include longitudinally extensive optic nerve lesions, spinal cord involvement, and brain lesions with cortical or deep gray matter involvement. Pathologically, MOGAD involves antibody-mediated demyelination without the astrocytopathy seen in AQP4-NMOSD.
Treatment typically involves high-dose corticosteroids for acute attacks, with some patients requiring long-term immunosuppression. Prognosis is generally better than AQP4-NMOSD but variable, with relapses potentially causing cumulative disability. Research continues to clarify its pathogenesis, optimal therapies, and long-term outcomes. MOGAD highlights the importance of antibody testing in refining CNS demyelinating disorder classifications.
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