Myeloid-derived Suppressor Cells
Myeloid-derived Suppressor Cells - Related Videos
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Preparation of Myeloid Derived Suppressor Cells (MDSC) from Naive and Pancreatic Tumor-bearing Mice using Flow Cytometry and Automated Magnetic Activated Cell Sorting (AutoMACS)
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Cited by 9 •
2012
This is a rapid and comprehensive method of immunophenotyping Myeloid Derived Suppressor Cells (MDSC) and enriching Gr-1+ leukocytes from mouse spleens. This method uses flow cytometry and AutoMACS Cell Sorting to enrich for viable Gr-1+ leukocytes prior to FACS sorting of MDSC for use in vivo and in vitro assays.
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Studying Interactions between Myeloid Cells and CAR T Cells In Vitro and In Vivo
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2025
Given the limited xenograft models available to study interactions between human CART and myeloid cells, we established in vitro and in vivo models to understand the impacts of human macrophages on CART cells. Findings can potentially be generalized to evaluate macrophage roles in the tumor microenvironment and test macrophage-targeted immunotherapies.
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Culture of myeloid dendritic cells from bone marrow precursors
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Cited by 22 •
2008
This video demonstrates the procedure for differentiating myeloid dendritic cells from mouse bone marrow. Isolation of mouse tibia and femur, and processing of bone marrow are demonstrated. Pictures demonstrating cell morphology before and after differentiation, and figures depicting cell phenotype and IL-12 production following maturation using CpG are shown.
09:07
Isolation of Myeloid Dendritic Cells and Epithelial Cells from Human Thymus
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Cited by 27 •
2013
This protocol details a method to isolate antigen presenting cells from human thymus via different steps of enzymatic digestion of the tissue followed by density centrifugation of the single cell suspension and finally magnetic and/or FACS sorting of the cell populations of interest.
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In Vitro and In Vivo Assessment of T, B and Myeloid Cells Suppressive Activity and Humoral Responses from Transplant Recipients
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Cited by 1 •
2017
Here, we present a protocol to induce tolerance in transplantation, and assess in vitro and in vivo the suppressive capacity of distinct cell subsets from the recipient and the immune status of the recipient toward donor or exogenous antigens.
FAQs
Arginase-1 and inducible nitric oxide synthase, or iNOS, impair immune-cell activity through complementary effects. Arginase-1 contributes to nutrient depletion, while iNOS generates immunosuppressive reactive nitrogen species. Together, these activities limit the effectiveness of antitumor T-cell and natural killer-cell responses, helping explain how MDSCs support immune evasion within tumors.
MDSC heterogeneity matters because this population is not uniform, and its functional state may influence how strongly it suppresses antitumor immunity. Consequently, simply counting these cells may not fully describe their biological impact. Cancer studies therefore consider both abundance and function when relating MDSCs to disease progression or evaluating their potential as biomarkers.
Beyond directly weakening T-cell and natural killer-cell activity, MDSCs can reinforce a tumor-supportive environment through regulatory signaling and inflammation. These effects connect immune suppression with broader changes that favor tumor progression. Examining both immune-cell inhibition and the surrounding inflammatory context gives cancer researchers a more complete view of MDSC-associated tumor biology.
Researchers may evaluate MDSC abundance and functional state as potential indicators of disease progression. Abundance describes how extensively these cells accumulate, whereas functional state addresses their suppressive activity. Considering both measurements is important because a large population and a highly suppressive population may provide different biological information about a tumor.
MDSCs are important in immunotherapy research because their suppressive activity can weaken the antitumor immune responses that treatment aims to restore or enhance. Studies therefore examine whether MDSC accumulation or activity is associated with resistance to immunotherapy. This links the cells to treatment outcome and makes them relevant targets for improving responses to cancer therapy.
Potential interventions focus on two complementary goals: reducing MDSC recruitment to tumors or suppressing the cells’ immunosuppressive activity after they accumulate. The rationale is to relieve pressure on antitumor immune cells rather than addressing tumor cells alone. In cancer research, these strategies are examined for their ability to improve responses to existing treatment.