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U.S.A."],"published-print":{"date-parts":[[2016,12,6]]},"abstract":"<jats:title>Significance<\/jats:title>\n                  <jats:p>The alternative renin\u2013angiotensin system pathway, the angiotensin (Ang)-(1\u20137)\/Mas axis, may counterbalance Ang II-mediated proinflammatory effects. To investigate the role of the Ang-(1\u20137)\/Mas axis in immune cell function and inflammatory diseases in vivo, we used two different chronic inflammatory animal models. Deletion of Mas affects macrophage function and phenotype independently of the underlying phagocyte stimulus and aggravates the clinical course of experimental autoimmune encephalomyelitis as well as atherosclerosis in mice by tipping the in vivo balance from M(IL-4+IL-13)- to M(LPS+IFN\u03b3)-like macrophages. 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