MOC1 Antibody
Description
Target Antigen and Mechanism
CD56/NCAM:
The MOC1 antibody binds to a specific isoform of CD56, enabling selective identification of CD56+ cells in diagnostic and research settings .
Diagnostic Uses
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Flow cytometry: Identification and quantification of NK cells in peripheral blood .
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Tissue typing: Critical for safe blood transfusion and organ transplantation .
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Cancer diagnostics: Detection of CD56+ tumors (e.g., neuroendocrine cancers) .
Research Applications
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Immune profiling: Analysis of NK cell populations in cancer and autoimmune diseases .
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Tumor microenvironment studies: Used alongside other markers to evaluate immune infiltration in murine oral squamous cell carcinoma (OSCC) models .
Comparative Analysis with Other CD56 Antibodies
While multiple CD56-targeting clones exist (e.g., NK1, 123C3), MOC-1 distinguishes itself through:
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Specific isoform recognition: Binds a 145 kDa NCAM variant, unlike clones targeting other isoforms .
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Robust performance in flow cytometry: Validated for high sensitivity in detecting NK cells .
Key Studies Involving MOC1 Antibody
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NK cell quantification: Used to identify reduced NK populations in autoimmune disorders .
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Tumor immunogenicity: Applied in murine OSCC models (MOC1 cell line) to correlate CD56 expression with immune evasion .
Data Highlights
Challenges and Limitations
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Species restriction: Murine origin limits therapeutic use in humans due to immunogenicity .
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Specificity constraints: Does not detect all NCAM isoforms, reducing utility in certain cancer subtypes .
Future Directions
Product Specs
**Constituents:** 50% Glycerol, 0.01M PBS, pH 7.4
Target Background
KEGG: ath:AT2G26840
UniGene: At.38840
Q&A
Basic Research Questions
How do MOC1 and MOC2 tumor models differ in baseline immunogenicity?
Methodological approach:
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MHC class I quantification: Use flow cytometry to compare constitutive/inducible H2-Kb/H2-Db expression (MOC1: 12× higher basal H2-Kb vs. MOC2; 2.5× IFNγ-inducible H2-Kb) .
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TIL profiling: Employ immunohistochemistry for CD8+/CD4+ T cells (MOC1: 3:1 CD8+:CD4+ ratio vs. MOC2: 1:2) .
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In vivo validation: Compare tumor growth in WT vs. RAG2−/− mice (MOC1 shows 40% slower growth in WT; p<0.01) .
Key data table:
| Parameter | MOC1 | MOC2 | Significance |
|---|---|---|---|
| Basal H2-Kb | 12× higher | Low | p<0.001 |
| CD8+ TIL density | 1,200 cells/mm² | 300 cells/mm² | p=0.004 |
| FOXP3+ Tregs | 5% of CD4+ | 22% of CD4+ | p=0.009 |
What experimental endpoints are optimal for assessing PD-L1 antibody efficacy in MOC1 models?
Protocol recommendations:
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Primary endpoint: Time to 750 mm³ tumor volume (log-rank analysis shows 90% rejection with R,R-CDG + PD-L1 mAb vs. 50% with monotherapy; p=0.041) .
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Immune correlates:
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Resistance markers: CXCR2+ PMN-MDSC infiltration (>15% myeloid cells predicts resistance; HR=2.8)
Advanced Research Questions
How to resolve contradictory data on mTOR/MEK inhibition synergism with PD-L1 antibodies?
Conflict analysis framework:
Resolution strategy:
What mechanisms drive adaptive resistance to PD-1 blockade in MOC1 variants?
Multi-omics approach:
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Clonal selection:
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T cell dynamics:
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Therapeutic bypass:
Validation metrics:
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Spatial transcriptomics confirming CXCL9 gradient (≥2-fold peri-tumoral vs. core)
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MDSC depletion via anti-Ly6G (1D8 clone) enhances NK cytotoxicity by 60%
Critical data contradiction note: While MOC1 shows baseline immunogenicity , its STING agonist response requires intact IFNβ signaling (STING−/− mice show 100% progression despite treatment) . Researchers must pre-screen for:
