CD170 antibody: How to block the tumor immune escape mechanism mediated by myeloid-derived suppressor cells?

CD170 antibody: How to block the tumor immune escape mechanism mediated by myeloid-derived suppressor cells?

1. What is the immunological significance of sialylation modifications in the tumor microenvironment?

Abnormal sialylation of glycans on tumor cell surfaces is a hallmark of cancer, promoting immune escape through multiple mechanisms. The sialylated glycosylation patterns can specifically bind to sialic acid-binding immunoglobulin-like lectin (Siglec) family receptors on immune cells. As an inhibitory Siglec receptor family member, CD170 transmits inhibitory signals through its intracellular immunoreceptor tyrosine-based inhibitory motifs (ITIMs). In the tumor microenvironment, this interaction forms an immunosuppressive network where the highly sialylated state of myeloid-derived suppressor cells (MDSCs) enhances their immunosuppressive capabilities through binding with CD170 receptors.

2. How is CD170 expressed and what functions does it perform in myeloid suppressor cells?

Studies show that CD170 is highly expressed in MDSCs from both lung cancer patients and mouse tumor models, correlating closely with their immunosuppressive functions. Genetic knockout of CD170 specifically in myeloid cells significantly delays tumor growth and promotes infiltration and activation of CD8+ T cells in tumor tissues. This demonstrates CD170's critical role in MDSC-mediated immune regulation and suggests its potential as a novel target for intervening in tumor immune escape.

3. What molecular pathways are involved in CD170-mediated immunosuppression?

CD170 regulates immune responses through multiple molecular mechanisms. Experimental evidence shows that blocking CD170-ligand interactions or reducing cell surface sialylation significantly attenuates MDSC-mediated T cell suppression. Mechanistically, CD170 activation upregulates chemokine CCL2 expression, which plays a crucial role in establishing the immunosuppressive microenvironment. Neutralizing CCL2 with specific antibodies can effectively reverse CD170-mediated immunosuppression and prolong survival in tumor-bearing animals, suggesting CCL2 as a key downstream effector molecule.

4. What potential value do CD170-targeted therapeutic strategies offer?

CD170-targeted interventions show promising prospects in cancer immunotherapy. Preclinical studies confirm that antibody blockade of CD170 or enzymatic removal of surface sialic acids can effectively restore T cell anti-tumor function. Notably, in human monocyte-derived MDSC models, CD170 blockade similarly reduces immunosuppression, indicating conserved mechanisms across species. These findings provide theoretical foundations for developing novel combination immunotherapy strategies.

5. How does CD170 synergize with other immune checkpoints?

The CD170-mediated immunosuppressive pathway may synergize with known immune checkpoint molecules. In the tumor microenvironment, multiple inhibitory receptors form a complex immunoregulatory network. Understanding cross-talk between CD170 and other checkpoints like PD-1 or CTLA-4 is crucial for designing effective combination therapies. Preliminary evidence suggests CD170 blockade may synergize with existing immune checkpoint inhibitors, offering new approaches to overcome immunotherapy resistance.

6. What challenges exist in future research directions and clinical translation?

Translating CD170-targeted therapies requires addressing several key challenges: First, clarifying CD170's expression dynamics and functional heterogeneity across tumor types and disease stages. Second, developing reliable biomarkers to predict treatment response. Third, optimizing antibody specificity, affinity, and pharmacokinetics. Considering immune system complexity, thoroughly understanding CD170's physiological functions is equally essential for assessing long-term treatment safety.

7. Conclusion

As a key immunoregulatory receptor on MDSCs, CD170 plays a crucial role in tumor immune escape by recognizing sialylated ligands and regulating chemokines like CCL2. Blocking CD170 signaling effectively reverses MDSC-mediated immunosuppression and enhances anti-tumor immunity. These findings deepen understanding of tumor microenvironment immunosuppression and provide promising targets for novel immunotherapy strategies. Further exploration of CD170 biology may open new avenues in cancer immunotherapy.

8. Which manufacturers provide CD170 antibodies?

Hangzhou Start Biotech Co., Ltd. has independently developed "Rat Anti-Mouse CD170 Antibody" (Product Name: Rat Anti-Mouse CD170 Antibody (S-R691), Catalog Number: S0B5103), a high-specificity, excellent-affinity, and exceptionally stable immunoregulatory receptor detection tool. This product precisely recognizes mouse CD170 (Siglec-E) protein, with significant applications in myeloid cell function studies, inflammatory response regulation, and tumor immune microenvironment exploration in mouse models.

Technical Support: We provide comprehensive product documentation including validation data, experimental protocols, and professional support to facilitate advancements in innate immunity and inflammation research.

Hangzhou Start Biotech Co., Ltd. is committed to providing high-quality, valuable biological reagents and solutions for global biopharma and research institutions. For more information about "Rat Anti-Mouse CD170 Antibody" (Catalog S0B5103) or sample requests, please contact us.

Product Information

S0B5084

Alexa Fluor® 647 Rat Anti-Mouse CD170 Antibody (S-R691)

Host : Rat

Conjugation : Alexa Fluor® 647

S0B5103

Rat Anti-Mouse CD170 Antibody (S-R691)

Host : Rat

Conjugation : Unconjugated