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Published on: January 20, 2019
CD301b lectin expression in the breast tumor microenvironment augments tumor growth
Ahmet Ozdilek1, Amy V Paschall1, Zahra Nawaz1
1Department of Biochemistry, Emory Vaccine Center, Winship Cancer Institute, Emory University School of Medicine, Atlanta, GA 30322.
Insights
Aberrant tumor glycosylation impacts immune recognition. Researchers found that the C-type lectin CD301b promotes breast tumor growth by interacting with myeloid cells, suggesting it as a therapeutic target.
Area of Science:
- Immunology
- Oncology
- Glycobiology
Background:
- Aberrant tumor glycosylation influences immune recognition, but its role in tumor progression via glycan-lectin interactions is unclear.
- The tumor microenvironment (TME) plays a critical role in cancer progression and immune evasion.
- C-type lectin receptors are key mediators of cell-cell interactions within the immune system.
Purpose of the Study:
- To investigate the role of C-type lectin receptor CD301b (encoded by *Mgl2*) in regulating immune activity within the breast tumor microenvironment.
- To elucidate the specific glycan-lectin interactions influencing tumor progression in breast cancer.
- To identify CD301b as a potential therapeutic target for reprogramming the breast cancer TME.
Main Methods:
- Utilized a murine triple-negative breast cancer model to study tumor growth and immune cell interactions.
- Employed CD301b depletion and genetic knockout strategies to assess its functional role.
- Conducted phenotypic analyses, single-cell RNA sequencing, and transcriptomic profiling of tumors.
Main Results:
- Tumors expressing the Tn glycoantigen exhibited accelerated growth, facilitated by CD301b-expressing immune cells.
- Depletion or genetic loss of CD301b significantly suppressed tumor growth, indicating its role in myeloid-tumor interactions.
- CD301b+ cells were identified as type 2 conventional dendritic cells (cDC2s), and its human ortholog CLEC10A is expressed in human cDC2-like cells and macrophages, suggesting conserved function.
- Mice deficient in *Mgl2* displayed tumors with an inflammatory, immune-activated phenotype, indicative of enhanced antitumor immunity.
Conclusions:
- CD301b acts as a crucial regulator of immune activity within the breast tumor microenvironment, promoting tumor progression.
- The study establishes a direct link between aberrant tumor glycosylation and lectin signaling in myeloid cells.
- CD301b represents a promising therapeutic target for modulating the tumor immune microenvironment and enhancing antitumor immunity in breast cancer.
Abstract:
Aberrant tumor glycosylation can alter immune recognition; however, the specific influence of glycan-lectin interactions on tumor progression remains poorly understood. Here, we identify the C-type lectin receptor CD301b (encoded by Mgl2) as a regulator of immune activity within the breast tumor microenvironment (TME). Using a murine triple-negative breast cancer model, we demonstrate that tumors expressing the Tn glycoantigen grow more rapidly, and this growth is facilitated by CD301b+ immune cells. Depletion or genetic loss of CD301b markedly suppressed tumor growth, indicating that CD301b promotes tumor progression through myeloid-tumor interactions. Phenotypic analyses revealed that CD301b+ cells within tumors are type 2 conventional dendritic cells (cDC2s), a subset known to influence immune polarization. Single-cell RNA sequencing of human breast cancers showed that the human ortholog CLEC10A is expressed in cDC2-like dendritic cells and select macrophage subsets, suggesting a conserved role for CD301+ myeloid populations. Transcriptomic profiling of tumors developed in Mgl2-deficient mice revealed a shift toward an inflammatory, immune-activated state consistent with enhanced antitumor immunity. Together, these findings establish a link between tumor glycosylation and lectin signaling of myeloid cells, highlighting CD301b as a potential target for reprogramming the tumor immune microenvironment in breast cancer.
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