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The specific mechanisms mediating immune deficiency in CVID remain to be determined. Previous studies indicated that immune dysregulation in CVID patients is associated with chronic microbial translocation, systemic immune activation, and altered homeostasis of lymphocytic and myeloid lineages. A detailed phenotypic, functional characterization of plasma markers and immune cell populations was performed in 46 CVID patients and 44 healthy donors. CVID patients displayed significantly elevated plasma levels of a marker of neutrophil activation neutrophil gelatinase\u2013associated lipocalin. Neutrophils from CVID patients exhibited elevated surface levels of CD11b and PD-L1 and decreased levels of CD62L, CD16, and CD80, consistent with a phenotype of activated neutrophils with suppressive properties. Neutrophils from CVID patients actively suppressed T cell activation and release of IFN-\u03b3 via the production of reactive oxygen species. Furthermore, CVID was associated with an increased frequency of low-density neutrophils (LDNs)\/granulocytic myeloid-derived suppressor cells. LDN\/granulocytic myeloid-derived suppressor cell frequency in CVID patients correlated with reduced T cell responsiveness. Exogenous stimulation of whole blood with bacterial LPS emulated some but not all of the phenotypic changes observed on neutrophils from CVID patients and induced neutrophil population with LDN phenotype. The presented data demonstrate that neutrophils in the blood of CVID patients acquire an activated phenotype and exert potent T cell suppressive activity. Specific targeting of myeloid cell\u2013derived suppressor activity represents a novel potential therapeutic strategy for CVID.<\/jats:p>","DOI":"10.4049\/jimmunol.1800102","type":"journal-article","created":{"date-parts":[[2018,11,28]],"date-time":"2018-11-28T20:54:21Z","timestamp":1543438461000},"page":"93-104","source":"Crossref","is-referenced-by-count":31,"title":["Neutrophil and Granulocytic Myeloid-Derived Suppressor Cell\u2013Mediated T Cell Suppression Significantly Contributes to Immune Dysregulation in Common Variable Immunodeficiency Disorders"],"prefix":"10.1093","volume":"202","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-2122-7784","authenticated-orcid":false,"given":"Marcela","family":"Vlkova","sequence":"first","affiliation":[{"name":"Department of Clinical Immunology and Allergology, Faculty of Medicine, Masaryk University , 625 00 Brno ,","place":["Czech Republic"]},{"name":"St. Anne\u2019s University Hospital , 656 91 Brno ,","place":["Czech 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