Myeloid‐derived suppressor cells: Roles and relations with Th2, Th17, and Treg cells in asthma

Allergy ◽  
2019 ◽  
Vol 74 (11) ◽  
pp. 2233-2237 ◽  
Author(s):  
Qingdong Guan ◽  
Bin Yang ◽  
Richard J. Warrington ◽  
Steven Mink ◽  
Chrystyna Kalicinsky ◽  
...  
Keyword(s):  
Suppressor Cells ◽  
Treg Cells ◽  
Myeloid Derived Suppressor Cells

scholarly journals Immunomodulation by Inflammation during Liver and Gastrointestinal Tumorigenesis and Aging

2021 ◽  
Vol 22 (5) ◽  
pp. 2238
Author(s):  
Nao Nagai ◽  
Yotaro Kudo ◽  
Daisuke Aki ◽  
Hayato Nakagawa ◽  
Koji Taniguchi
Keyword(s):  
Colorectal Cancer ◽  
Chronic Inflammation ◽  
Antitumor Immunity ◽  
Suppressor Cells ◽  
Treg Cells ◽  
Cytotoxic T Cell ◽  
Myeloid Derived Suppressor Cells ◽  
Age Related ◽  
Immunosuppressive Tumor Microenvironment ◽  
Pro Inflammatory Cytokines

Chronic inflammation is thought to promote tumorigenesis and metastasis by several mechanisms, such as affecting tumor cells directly, establishing a tumor-supporting microenvironment, enhancing tumor angiogenesis, and suppressing antitumor immunity. In this review, we discuss the recent advances in our understanding of how inflammation induces the immunosuppressive tumor microenvironment, such as increasing the level of pro-inflammatory cytokines, chemokines, and immunosuppressive molecules, inducing immune checkpoint molecules and cytotoxic T-cell exhaustion, and accumulating regulatory T (Treg) cells and myeloid-derived suppressor cells (MDSCs). The suppression of antitumor immunity by inflammation is especially examined in the liver and colorectal cancer. In addition, chronic inflammation is induced during aging and causes age-related diseases, including cancer, by affecting immunity. Therefore, we also discuss the age-related diseases regulated by inflammation, especially in the liver and colon.

scholarly journals The Clinical Significance of Programmed Death-1, Regulatory T Cells and Myeloid Derived Suppressor Cells in Patients with Nontuberculous Mycobacteria-Lung Disease

2019 ◽  
Vol 8 (5) ◽  
pp. 736 ◽  
Author(s):  
Chin-Chung Shu ◽  
Sheng-Wei Pan ◽  
Jia-Yih Feng ◽  
Jann-Yuan Wang ◽  
Yu-Jiun Chan ◽  
...  
Keyword(s):  
Lung Disease ◽  
Radiographic Progression ◽  
Cytotoxic T Lymphocyte ◽  
Nontuberculous Mycobacteria ◽  
Suppressor Cells ◽  
Treg Cells ◽  
Myeloid Derived Suppressor Cells ◽  
Programmed Death ◽  
Programmed Death 1 ◽  
Cd4 Lymphocytes

Background: Increasing expression of programmed death-1 (PD-1) in patients with nontuberculous mycobacteria lung disease (NTM-LD) has been reported, but its role in clinical characteristics and outcomes remains unclear. Methods: We enrolled 96 participants, including 46 with Mycobacterium avium complex (MAC)-LD, 23 with M. abscessus (MAB)-LD, and 27 controls. We measured expressions of PD-1, cytotoxic T-lymphocyte antigen-4 (CTLA-4) and regulatory T (Treg) cells on CD4+ lymphocytes and myeloid-derived suppressor cells (MDSCs) and analyzed their association with clinical features and radiographic outcomes. Results: The percentage of PD-1 on CD4+(PD-1+CD4+) lymphocytes and MDSCs were higher in the MAC-LD group than the controls. There were no intergroup differences regarding CTLA-4+CD4+ lymphocytes. Higher PD-1+CD4+ lymphocytes were found in M. intracellulare- and M. avium-LD than in other MAC-LD. Positive sputum acid-fast stains and fibrocavitary radiographic lesions were correlated with elevated PD-1+CD4+ lymphocytes and Treg cells. The percentage of PD-1+CD4+ lymphocytes at the initial and 2 months of follow-up significantly predicted subsequent radiographic progression. Conclusion: As markers of immune tolerance, PD-1+CD4+ lymphocytes and MDSCs were higher in MAC-LD patients. The levels of PD-1+CD4+ and Treg cells were correlated with high mycobacteria bacilli burden in NTM-LD. Monitoring the expressions of PD-1+CD4+ lymphocytes may predict radiographic progression.

scholarly journals Programmed Death-Ligand 1 Expression Potentiates the Immune Modulatory Function Of Myeloid-Derived Suppressor Cells in Systemic Lupus Erythematosus

2021 ◽  
Vol 12 ◽  
Author(s):  
Min-Jung Park ◽  
Jin-Ah Baek ◽  
Jeong Won Choi ◽  
Se Gwang Jang ◽  
Da-Som Kim ◽  
...  
Keyword(s):  
T Cells ◽  
Lupus Erythematosus ◽  
Suppressor Cells ◽  
Treg Cells ◽  
Mrna Levels ◽  
Myeloid Derived Suppressor Cells ◽  
Programmed Death Ligand 1 ◽  
Follicular Helper ◽  
Programmed Death ◽  
Models Of Lupus

Multiple studies have explored the potential role of programmed death-ligand 1 (PD-L1) as a mediator of Myeloid-derived suppressor cells (MDSCs) effects in various cancers. However, the role PD-L1 expression in MDSCs on autoimmune disease is still largely unknown.This study was undertaken to whether MDSC expressing PD-L1 have more potent immunoregulatory activity and control autoimmunity more effectively in two murine models of lupus (MRL/lpr mice and Roquinsan/san mice). The populations of MDSC were increased in peripheral blood of lupus patients. The mRNA levels of immunosuppressive molecules were profoundly decreased in MDSCs from lupus patients and mice. Co-culture with splenocytes showed that PD-L1 expressing MDSCs from control mice expand both Treg cells and regulatory B cells more potently. Infusion of PD-L1 expressing MDSCs reduced autoantibody levels and degree of proteinuria and improved renal pathology of two animal models of lupus. Moreover, PD-L1 expressing MDSCs therapy can suppress double negative (CD4-CD8-CD3+) T cells, the major pathogenic immune cells and follicular helper T cells in MRL/lpr mice, and podocyte damage. Our results indicate PD-L1 expressing MDSCs have more potent immunoregualtory activity and ameliorate autoimmunity more profoundly. These findings suggest PD-L1 expressing MDSCs be a promising therapeutic strategy targeting systemic autoimmune diseases.

scholarly journals Artepillin C Reduces Allergic Airway Inflammation by Induction of Monocytic Myeloid-Derived Suppressor Cells

Pharmaceutics ◽  
2021 ◽  
Vol 13 (11) ◽  
pp. 1763
Author(s):  
Núbia Sabrina Martins ◽  
Thais Fernanda de Campos Fraga-Silva ◽  
Giseli Furlan Correa ◽  
Mèdéton Mahoussi Michaël Boko ◽  
Leandra Naira Zambelli Ramalho ◽  
...  
Keyword(s):  
Airway Inflammation ◽  
Allergic Asthma ◽  
Allergic Airway Inflammation ◽  
Suppressor Cells ◽  
Treg Cells ◽  
Transfer Model ◽  
Myeloid Derived Suppressor Cells ◽  
Asthma Model ◽  
Artepillin C ◽  
Anti Inflammatory

Propolis is a natural product produced by bees that is primarily used in complementary and alternative medicine and has anti-inflammatory, antibacterial, antiviral, and antitumoral biological properties. Some studies have reported the beneficial effects of propolis in models of allergic asthma. In a previous study, our group showed that green propolis treatment reduced airway inflammation and mucus secretion in an ovalbumin (OVA)-induced asthma model and resulted in increased regulatory T cells (Treg) and polymorphonuclear myeloid-derived suppressor cells (PMN-MDSC) frequencies in the lungs, two leukocyte populations that have immunosuppressive functions. In this study, we evaluated the anti-inflammatory effects of artepillin C (ArtC), the major compound of green propolis, in the context of allergic airway inflammation. Our results show that ArtC induces in vitro differentiation of Treg cells and monocytic MDSC (M-MDSC). Furthermore, in an OVA-induced asthma model, ArtC treatment reduced pulmonary inflammation, eosinophil influx to the airways, mucus and IL-5 secretion along with increased frequency of M-MDSC, but not Treg cells, in the lungs. Using an adoptive transfer model, we confirmed that the effect of ArtC in the reduction in airway inflammation was dependent on M-MDSC. Altogether, our data show that ArtC exhibits an anti-inflammatory effect and might be an adjuvant therapy for allergic asthma.

Modulation of regulatory T cells and myeloid-derived suppressor cells by sorafenib and sunitinib in renal cell carcinoma patients

2009 ◽  
Vol 27 (15_suppl) ◽  
pp. e16002-e16002
Author(s):  
A. Floercken ◽  
A. Takvorian ◽  
A. Singh ◽  
W. Hopfenmüller ◽  
A. Pezzutto ◽  
...  
Keyword(s):  
T Cells ◽  
Renal Cell ◽  
Kinase Inhibitors ◽  
Cell Cancer ◽  
Suppressor Cells ◽  
Treg Cells ◽  
Negative Influence ◽  
Myeloid Derived Suppressor Cells ◽  
Major Mechanism ◽  
Hla Dr

e16002 Background: Induction of regulatory T (Treg) and myeloid-derived suppressor cells (MDSC) is a major mechanism for the escape of tumors from immunological control. Increased levels of Treg cells have been described in renal cell cancer (RCC) patients and seem to correlate with an adverse outcome. Furthermore, reduction of Treg has been reported for RCC patients under sunitinib therapy. The aim of our study was to analyse the influence of sorafenib and sunitinib on the frequency of Treg and MDSC in patients with metastatic RCC (mRCC). Methods: The number of T reg, MDSC and lymphocyte subpopulations was analysed by flowcytometry in peripheral blood (pb) of patients (n=19) with histologically confirmed mRCC under treatment with either sunitinib (50 mg/d, n=11) or sorafenib (800 mg/d, n=8). After informed consent blood samples were taken before and during the 1st, 2nd, and 3rd month of therapy. Flowcytometric analysis was performed using fluorochrome labeled antibodies against CD3, CD4, CD8, CD25, CD127, FOXp3, CD33, C14, CD11b and HLA-DR. Results: The baseline level of Treg did not differ from healthy controls. However, there was a significant increase of CD3+CD4+CD25+FOXp3+Treg (13,5% vs. 36,3% of gated cells, p= 0.02) and the ratio FOXp3+/FOXp3- CD3+CD4+ T cells (0,16% vs. 0,56% of gated cells, p= 0.02) in the group of sorafenib-treated patients compared to sunitinib-treated patients during the 1st month of therapy and thereafter. This effect was confirmed in an intragroup analysis. There was no influence of Sunitinib on the frequency of Treg. Analysis of CD33+/HLA-DR-/11b+ MDSC did not reveal any change under treatment with sorafenib or sunitinib. Conclusions: Sorafenib, but not sunitinib, leads to an early and sustained increase of Treg in pb of mRCC patients. A negative influence of sorafenib on primary immune responses has been described and has mainly been attributed to functional impairment of dendritic cells (DC). Whether altered DC function under sorafenib is responsible for the induction of Treg in RCC patients will have to be addressed in future studies. In immunoresponsive tumors such as RCC, immunological effects of kinase inhibitors are particularly relevant for the design of combination trials with immunotherapeutic agents. No significant financial relationships to disclose.

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