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In the present study, the number and immunosuppressive activity of MDSCs isolated from na\u00efve\n                    <jats:italic>\n                      Il10\n                      <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    <\/jats:italic>\n                    ,\n                    <jats:italic>\n                      Il17\n                      <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    <\/jats:italic>\n                    , and WT mice as control, as well as from house dust mite extract (HDM)\u2010induced asthmatic\n                    <jats:italic>\n                      Il10\n                      <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    <\/jats:italic>\n                    and\n                    <jats:italic>\n                      Il17\n                      <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    <\/jats:italic>\n                    mice, were investigated. IL\u201010 deficiency increased the number of polymorphonuclear (PMN)\u2010MDSCs in the lung, spleen, and bone marrow, without concurrent impairment of their suppressive activity in vitro. In the asthma model, the IL\u201017 knockout was concomitant with a lower number and activity of monocytic (M)\u2010MDSCs and an altered inflammatory reaction with impaired lung function. Additionally, we found a higher baseline inflammation of the\n                    <jats:italic>\n                      Il17\n                      <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    <\/jats:italic>\n                    mice in the lung, manifested in increased airway resistance. We conclude that the impact of IL\u201010 and IL\u201017 deficiency on MDSCs differs in the context of inflammation. Accordingly, the in vitro experiments demonstrated an increased number of PMN\u2010MDSCs across tissues in\n                    <jats:italic>\n                      Il10\n                      <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    <\/jats:italic>\n                    mice, which indicates that IL\u201010 might serve a pivotal role in preserving immune homeostasis under physiological circumstances. In the context of HDM\u2010induced airway inflammation, IL\u201017 was found to be an important player in the suppression of pulmonary inflammation and regulation of M\u2010MDSCs.\n                  <\/jats:p>","DOI":"10.1002\/eji.202350785","type":"journal-article","created":{"date-parts":[[2024,4,24]],"date-time":"2024-04-24T01:00:10Z","timestamp":1713920410000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":4,"title":["The impact of IL\u201010 and IL\u201017 on myeloid\u2010derived suppressor cells\n                    <i>in vitro<\/i>\n                    and\n                    <i>in vivo<\/i>\n                    in a murine model of asthma"],"prefix":"10.1002","volume":"54","author":[{"given":"Charlotte","family":"Vetter","sequence":"first","affiliation":[{"name":"Institute of Laboratory Medicine member of the German Center for Lung Research (DZL) Universities of Giessen and Marburg Lung Center (UGMLC) Philipps 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