The resMφs bring about postresolution lymphocyte contraction in an iNOS-dependent manner. The resMφs from 0.1 mg of zymosan and S pneumonia-induced acute resolving inflammation revealed increased expression of (A) iNOS and (B) arginase. (C) Immunofluorescence was used to visualize the intracellular localization of iNOS in postresolution resMφs, whereas (D) confirmed their iNOS-dependent suppression of T-cell proliferation. (E) Some PKH26-PCL^red-positive resMφs migrate to mesenteric lymph nodes and spleen day 9 post 0.1 mg zymosan. Migrated iNOS-expressing resMφs mediate immune suppression was illustrated in iNOS^−/− mice, although the composition of the (F) naïve cavity is equivalent between knockouts and controls, and 14 days after inflammation lymphocyte numbers were greater in iNOS^−/− mice (G) peritoneal cavity and (H) spleens with (I) effects in persisting in spleen for up to 6 weeks. (G-I) The reversal of adaptive immune responses in iNOS deficient animals by the intraperitoneal injection of PKH26-PCL^red-positive resMφ from WT mice into iNOS^−/− mice are shown. (J) Adoptively transferred resMφs (stained red) from WT mice migrated to the spleen of iNOS knockouts; CD3 cells are stained in green. The P value was ≤.05, as determined by ANOVA, followed by the Bonferroni t test or two-tailed Student t test, with data expressed as mean ± SEM for n = 6 mice/group. *P ≤ .05; **P < .01; ***P < .001.