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Review
. 2021 Sep 21:12:745326.
doi: 10.3389/fimmu.2021.745326. eCollection 2021.

Granulocytic Myeloid-Derived Suppressor Cells in Cystic Fibrosis

Affiliations
Review

Granulocytic Myeloid-Derived Suppressor Cells in Cystic Fibrosis

Samantha L Tucker et al. Front Immunol. .

Abstract

Cystic Fibrosis (CF) is a genetic disease that causes chronic and severe lung inflammation and infection associated with high rates of mortality. In CF, disrupted ion exchange in the epithelium results in excessive mucus production and reduced mucociliary clearance, leading to immune system exacerbation and chronic infections with pathogens such as P. aeruginosa and S. aureus. Constant immune stimulation leads to altered immune responses including T cell impairment and neutrophil dysfunction. Specifically, CF is considered a Th17-mediated disease, and it has been proposed that both P. aeruginosa and a subset of neutrophils known as granulocytic myeloid suppressor cells (gMDSCs) play a role in T cell suppression. The exact mechanisms behind these interactions are yet to be determined, but recent works demonstrate a role for arginase-1. It is also believed that P. aeruginosa drives gMDSC function as a means of immune evasion, leading to chronic infection. Herein, we review the current literature regarding immune suppression in CF by gMDSCs with an emphasis on T cell impairment and the role of P. aeruginosa in this dynamic interaction.

Keywords: cystic fibrosis; gMDSC; immunosuppression; myeloid-derived suppressor cell; neutrophil.

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Conflict of interest statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Figures

Figure 1
Figure 1
General and CF-specific features of gMDSCs. Surface markers and intracellular molecules are indicated that have higher expressions or activities in granulocytic MDSCs in general (left panel) or in gMDSCs in CF (right panel).

References

    1. Rommens JM, Iannuzzi MC, Kerem B, Drumm ML, Melmer G, Dean M, et al. . Identification of the Cystic Fibrosis Gene: Chromosome Walking and Jumping. Science (1989) 245(4922):1059–65. doi: 10.1126/science.2772657 - DOI - PubMed
    1. Yoshimura K, Nakamura H, Trapnell BC, Chu CS, Dalemans W, Pavirani A, et al. . Expression of the Cystic Fibrosis Transmembrane Conductance Regulator Gene in Cells of non-Epithelial Origin. Nucleic Acids Res (1991) 19(19):5417–23. doi: 10.1093/nar/19.19.5417 - DOI - PMC - PubMed
    1. Trapnell BC, Chu CS, Paakko PK, Banks TC, Yoshimura K, Ferrans VJ, et al. . Expression of the Cystic Fibrosis Transmembrane Conductance Regulator Gene in the Respiratory Tract of Normal Individuals and Individuals With Cystic Fibrosis. Proc Natl Acad Sci USA (1991) 88(15):6565–9. doi: 10.1073/pnas.88.15.6565 - DOI - PMC - PubMed
    1. Khan MA, Ali ZS, Sweezey N, Grasemann H, Palaniyar N. Progression of Cystic Fibrosis Lung Disease From Childhood to Adulthood: Neutrophils, Neutrophil Extracellular Trap (NET) Formation, and NET Degradation. Genes (Basel) (2019) 10(3). doi: 10.3390/genes10030183 - DOI - PMC - PubMed
    1. Margaroli C, Garratt LW, Horati H, Dittrich AS, Rosenow T, Montgomery ST, et al. . Elastase Exocytosis by Airway Neutrophils Is Associated With Early Lung Damage in Children With Cystic Fibrosis. Am J Respir Crit Care Med (2019) 199(7):873–81. doi: 10.1164/rccm.201803-0442OC - DOI - PMC - PubMed

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