<scp>CD</scp>11b+Gr‐1<sup>dim</sup> Tolerogenic Dendritic Cell–Like Cells Are Expanded in Interstitial Lung Disease in <scp>SKG</scp> Mice

Sendo, Sho; Saegusa, Jun; Okano, T.; Takahashi, S.; Akashi, Koichi; Morinobu, Akio

doi:10.1002/art.40231

Cited by 22 publications

(22 citation statements)

References 45 publications

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“…We recently reported that MDSCs are expanded in the lungs of SKG mice with interstitial lung disease (ILD) [ 27 ]. Other researchers demonstrated that CCR2 + M-MDSCs inhibit collagen degradation and promote lung fibrosis by producing transforming growth factor-β1 (TGF-β1) [ 28 ].…”

Section: Main Textmentioning

confidence: 99%

Myeloid-derived suppressor cells in non-neoplastic inflamed organs

2018

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BackgroundMyeloid-derived suppressor cells (MDSCs) are a highly heterogeneous population of immature myeloid cells with immunosuppressive function. Although their function in tumor-bearing conditions is well studied, less is known about the role of MDSCs in various organs under non-neoplastic inflammatory conditions.Main bodyMDSCs are divided into two subpopulations, G-MDSCs and M-MDSCs, and their distribution varies between organs. MDSCs negatively control inflammation in inflamed organs such as the lungs, joints, liver, kidneys, intestines, central nervous system (CNS), and eyes by suppressing T cells and myeloid cells. MDSCs also regulate fibrosis in the lungs, liver, and kidneys and help repair CNS injuries. MDSCs in organs are plastic and can differentiate into osteoclasts and tolerogenic dendritic cells according to the microenvironment under non-neoplastic inflammatory conditions.ConclusionThis article summarizes recent findings about MDSCs under inflammatory conditions, especially with respect to their function and differentiation in specific organs.

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Section: Main Textmentioning

confidence: 99%

Myeloid-derived suppressor cells in non-neoplastic inflamed organs

2018

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“…Interestingly, the highest expression protein pattern of Gr-1+/CD44+ (Gr-1+ bright /CD44+ bright ) within the CD11b+ subset was associated with early cancer disease in the blood of cisplatin treated 4T1 tumorous mice. The Gr-1+ dim /CD44+ dim immature myeloid cells have been reported to suppress T-cells and IFN-γ production [37,38], the dim expression intensity of these markers was characteristic to 4T1 tumor bearing mice (Figure 8). In line with this, the smaller population of IFN-γ producing myeloid cells appeared within the CD11 subtype by cisplatin treatment which was completely absent in the advanced cancer ( Figure 8).…”

Section: Cisplatin Could Not Completely Restore the Peripheral Immunomentioning

confidence: 95%

Single Cell Mass Cytometry Revealed the Immunomodulatory Effect of Cisplatin Via Downregulation of Splenic CD44+, IL-17A+ MDSCs and Promotion of Circulating IFN-γ+ Myeloid Cells in the 4T1 Metastatic Breast Cancer Model

Balog

Hackler²,

Kovács³

et al. 2019

IJMS

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The treatment of metastatic breast cancer remained a challenge despite the recent breakthrough in the immunotherapy regimens. Here, we addressed the multidimensional immunophenotyping of 4T1 metastatic breast cancer by the state-of-the-art single cell mass cytometry (CyTOF). We determined the dose and time dependent cytotoxicity of cisplatin on 4T1 cells by the xCelligence real-time electronic sensing assay. Cisplatin treatment reduced tumor growth, number of lung metastasis, and the splenomegaly of 4T1 tumor bearing mice. We showed that cisplatin inhibited the tumor stroma formation, the polarization of carcinoma-associated fibroblasts by the diminished proteolytic activity of fibroblast activating protein. The CyTOF analysis revealed the emergence of CD11b+/Gr-1+/CD44+ or CD11b+/Gr-1+/IL-17A+ myeloid-derived suppressor cells (MDSCs) and the absence of B220+ or CD62L+ B-cells, the CD62L+/CD4+ and CD62L+/CD8+ T-cells in the spleen of advanced cancer. We could show the immunomodulatory effect of cisplatin via the suppression of splenic MDSCs and via the promotion of peripheral IFN-γ+ myeloid cells. Our data could support the use of low dose chemotherapy with cisplatin as an immunomodulatory agent for metastatic triple negative breast cancer.

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“…34,35 In this context, local lung epithelial DC function is suppressed by transforming growth factor-β (TGFβ), promoting immune tolerance, while others such as granulocyte macrophage colony stimulating factor (GM-CSF) promote DCmediated inflammation and autoimmunity. [35][36][37] Exactly how tobacco smoke may induce autoimmunity is not clear. It is composed of many chemicals, of which polycyclic aromatic hydrocarbons (PAHs) are known to activate the aryl hydrocarbon receptor, which is upregulated in RA synovial tissues.…”

Section: Pathobiology Of Rheumatoid Arthritis Lung Diseasementioning

confidence: 99%

“…38 Mice that are aryl hydrocarbon receptor deficient are resistant to collagen-induced arthritis and have attenuated Th17 immunity. 37 Peptidylarginine deiminase (PAD) enzymes regulate the conversion of peptidylarginine to peptidylcitrulline in a calcium-dependent reaction referred to as citrullination. PAD2 levels in the upper and lower airways are elevated in smokers, who also have higher levels of citrullinated peptides in BAL cells.…”

Section: Pathobiology Of Rheumatoid Arthritis Lung Diseasementioning

confidence: 99%

Pulmonary Complications of Rheumatoid Arthritis

Farquhar

Vassallo

Edwards

et al. 2019

Semin Respir Crit Care Med

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Rheumatoid arthritis (RA) is a common chronic autoimmune disorder that characteristically causes joint inflammation and damage. In addition, many patients develop extraarticular manifestations which may cause significant comorbidity and premature mortality.Some respiratory tract involvement of the upper and lower airways and parenchymal disease features are unique to RA, including cricoarytenoid arthritis and RA pulmonary nodulosis, and others, especially the interstitial parenchymal involvement, occur in many other idiopathic and autoimmune diseases. The pathophysiology of lung disease is not well understood. Rheumatoid lung disease may even predate the onset of joint disease, and could be triggered by chronic airway and alveolar epithelial injury. Chronic systemic inflammation and risk factors such as cigarette smoking, infection, host genetics, and immune dysregulation are contributors. Treatment of the respiratory disease is directed at reducing the systemic inflammation of RA. Less well understood is the management of the interstitial lung disease of RA, for which antifibrotic and immune suppressive agents may be helpful. The management of RA-related lung disease is perhaps the major remaining hurdle in reduction of the disease burden related to extraarticular manifestations of this disease.

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CD11b+Gr‐1^dim Tolerogenic Dendritic Cell–Like Cells Are Expanded in Interstitial Lung Disease in SKG Mice

Abstract: We identified unique suppressive myeloid cells that were differentiated from monocytic MDSCs in SKG mice with ILD, and we termed them CD11b+Gr-1 tolerogenic DC-like cells.

Cited by 22 publications

References 45 publications

Myeloid-derived suppressor cells in non-neoplastic inflamed organs

Myeloid-derived suppressor cells in non-neoplastic inflamed organs

Single Cell Mass Cytometry Revealed the Immunomodulatory Effect of Cisplatin Via Downregulation of Splenic CD44+, IL-17A+ MDSCs and Promotion of Circulating IFN-γ+ Myeloid Cells in the 4T1 Metastatic Breast Cancer Model

Pulmonary Complications of Rheumatoid Arthritis

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CD11b+Gr‐1dim Tolerogenic Dendritic Cell–Like Cells Are Expanded in Interstitial Lung Disease in SKG Mice

Abstract: We identified unique suppressive myeloid cells that were differentiated from monocytic MDSCs in SKG mice with ILD, and we termed them CD11b+Gr-1 tolerogenic DC-like cells.

Cited by 22 publications

References 45 publications

Myeloid-derived suppressor cells in non-neoplastic inflamed organs

Myeloid-derived suppressor cells in non-neoplastic inflamed organs

Single Cell Mass Cytometry Revealed the Immunomodulatory Effect of Cisplatin Via Downregulation of Splenic CD44+, IL-17A+ MDSCs and Promotion of Circulating IFN-γ+ Myeloid Cells in the 4T1 Metastatic Breast Cancer Model

Pulmonary Complications of Rheumatoid Arthritis

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CD11b+Gr‐1^dim Tolerogenic Dendritic Cell–Like Cells Are Expanded in Interstitial Lung Disease in SKG Mice