Distinct mechanisms govern populations of myeloid-derived suppressor cells in chronic viral infection and cancer
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View abstract on PubMed
Summary
This summary is machine-generated.Myeloid-derived suppressor cells (MDSCs) mechanisms differ between cancer and LCMV infection. Targeting ER stress for PMN-MDSCs and IFN-γ/IL-6 for M-MDSCs is key for immune restoration.
Area Of Science
- Immunology
- Cancer Biology
- Virology
Background
- Myeloid-derived suppressor cells (MDSCs) are critical regulators of immune responses in cancer and chronic infections.
- Understanding the specific mechanisms controlling MDSC activity across different diseases is essential for developing effective immunotherapies.
Purpose Of The Study
- To compare the regulatory mechanisms of MDSC activity in mouse models of cancer and lymphocytic choriomeningitis virus (LCMV) infection.
- To investigate the role of endoplasmic reticulum (ER) stress and cytokine signaling in MDSC function.
Main Methods
- Comparative analysis of monocytic MDSCs (M-MDSCs) and polymorphonuclear MDSCs (PMN-MDSCs) in cancer and LCMV-infected mice.
- Investigated the involvement of IRE1α, ATF6, IFN-γ, and IL-6 pathways in MDSC suppressive functions.
- Assessed the impact of blocking ER stress pathways on anti-tumor immunity.
Main Results
- LCMV infection induced M-MDSCs but not PMN-MDSCs, while both were present in cancer.
- PMN-MDSC suppressive activity in cancer was dependent on ER stress pathways (IRE1α, ATF6).
- M-MDSC suppressive activity was mediated by IFN-γ in spleens and IL-6 in tumors, with ER stress being dispensable for M-MDSCs.
Conclusions
- MDSC regulation involves distinct, disease- and population-specific mechanisms.
- Targeting ER stress in PMN-MDSCs and specific cytokine pathways in M-MDSCs offers potential strategies for immune modulation in cancer and infection.
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