MOG 37-46
MOG 37-46 is a dominant immunodominant CD8+ T cell epitope. As a truncated version of MOG35-55, MOG 37-46 is recognizable by MOG 35-55-specific T cells, and serves as an autoantibody target at the dimer interface of the extracellular domain of myelin oligodendrocyte glycoprotein (MOG). MOG 37-46 stimulates MOG-specific CD8+ T cell lines and proinflammatory CD8+ T cells migrating into the central nervous system (CNS) to produce IFN-γ. MOG 37-46 is applicable to research related to experimental autoimmune encephalomyelitis.
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- CAS 番号: 1235835-17-2
- 分子式: C59H83N17O14
- 分子量:1254.40
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保管条件:
Please store the product under the recommended conditions in the Certificate of Analysis.
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生物活性
製品説明
体外実験
MOG 37-46 (100 μM; 2 h) binds to H-2Db on RMA-S cells with relatively low but detectable affinity[1].
MOG37-46 (1-100 μM; 5 h-2 weeks) is the dominant CD8+ T cell epitope recognized by in vitro expanded lymph node-derived CD8+ T cells expanded with MOG35-55 peptide[2].
MOG37-46 (100 μM; 5 h) is the dominant CD8+ T cell epitope recognized by in vitro expanded lymph node-derived CD8+ T cells expanded with recombinant MOG protein, inducing IFNγ production in a higher percentage of cells than MOG44-54[2].
MOG37-46 (10-100 μM; 2 weeks) is recognized by in vitro expanded MOG37-46 reactive CD8+ T cell lines expanded with MOG37-46 peptide, which exhibit low functional avidity, requiring 100 μM MOG37-46 peptide for peak IFNγ production, which is 1000-fold higher than the concentration needed for viral antigen reactive CD8+ T cells[2].
MOG37-46 (10-100 μM; 5 h-2 weeks) is recognized by in vitro expanded MOG37-46 reactive CD8+ T cell lines expanded with MOG37-46 peptide, which are polyclonal, pro-inflammatory effector cells, producing IFNγ, TNFα, and IL-2 in response to 100 μM MOG37-46 peptide[2].
MOG 37-46 resides within the biologically relevant head-to-tail dimer interface of the mouse MOG extracellular domain, as determined via 1.8-Å resolution X-ray crystallography[3].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
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Cell Line:in vitro expanded lymph node-derived CD8+ T cell lines (expanded with MOG37-46 peptide)
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Concentration:10 μM (2 week in vitro expansion); 100 μM (peak IFNγ production restimulation)
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Incubation Time:2 weeks (in vitro expansion)
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Result:Induced peak IFNγ production at 100 μM, with reactive CD8+ T cells only responding to antigen at micromolar concentrations.
Exhibited 1000-fold lower avidity compared to viral antigen (GP33-43) reactive CD8+ T cells, which respond at nanomolar concentrations.
体内実験
MOG 37-46 (200 μg; s.c.; on days 0 and 7) induces severe EAE in female C57BL/6 mice with 100% incidence and equivalent clinical severity to the full-length MOG 35-55 peptide by day 23 post-immunization[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:C57BL/6 (female, 5-8 weeks of age, EAE induced by subcutaneous immunization with peptide emulsified in CFA and intraperitoneal pertussis toxin administration)[1]
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Dosage:200 μg
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Administration:s.c.; on days 0 and 7
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Result:Induced EAE with 100% disease incidence by day 23 post-immunization.
Exhibited mean clinical severity equivalent to mice immunized with MOG 35-55 or MOG 37-50 by day 23 post-immunization.
Showed slightly slower disease onset kinetics compared to MOG 35-55-immunized mice, but final average disease score matched other encephalitogenic peptide groups.
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Animal Model:C57BL/6 (female, 5-8 weeks of age, immunization-induced experimental autoimmune encephalomyelitis)[2]
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Dosage:100 µg
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Administration:s.c.; on days 0 and 7
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Result:Induced a chronic form of EAE with symptoms stabilizing around day 16 post-induction.
Reached an average peak clinical score of approximately 1.2.
Reduced CNS infiltration by CD4+ and CD8+ T cells (fewer than 1000 CD4+ T cells detected at any time point, with very small numbers of CD8+ T cells).
Showed a transient increase in macrophage infiltration observed at day 15.
Reduced activation of infiltrating macrophages and resident microglia, measured by MHC class I and class II expression, compared to MOG35-55-immunized mice.
化学情報
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CAS 番号 1235835-17-2
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分子量 1254.40
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分子式 C59H83N17O14
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配列
Val-Gly-Trp-Tyr-Arg-Ser-Pro-Phe-Ser-Arg
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シーケンスの短縮
VGWYRSPFSR
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輸送条件
Room temperature in continental US; may vary elsewhere.
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保管条件
Please store the product under the recommended conditions in the Certificate of Analysis.
プロトコル
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Research Protocol for Cancer Immunology
Cancer immunology studies how the immune system recognizes, suppresses, edits, or fails to eliminate malignant cells through tumor antigen release, antigen presentation, T-cell priming, immune trafficking, tumor-cell killing, and feedback inhibition in the tumor microenvironment. The cancer-immunity cycle links tumor antigenicity, dendritic-cell priming, CD8+ T-cell infiltration, cytotoxic function, and immune-checkpoint regulation to tumor rejection or immune escape. Immune-checkpoint pathways such as PD-1/PD-L1 and CTLA-4 suppress antitumor T-cell activity and can be therapeutically blocked, but many tumors remain resistant because of poor antigen presentation, weak T-cell infiltration, suppressive myeloid cells, regulatory T cells, and tumor-intrinsic immune-exclusion programs. Unresolved questions include which immune-cell states predict response, how tumor-intrinsic pathways exclude immune cells, how myeloid suppression limits checkpoint blockade, and which combination strategies
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参考文献
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MOG 37-46 関連分類
HY-P11796 関連分類
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