Interleukin (IL)-25, a Th2-related factor, inhibits the synthesis of inflammatory cytokines by macrophages and attenuates experimental colitis in mice. The mechanism underlying the counterregulatory effect of IL-25, however, remains unknown. Since Th2-cytokines can abrogate inflammatory pathways by inducing alternatively activated macrophages (AAMs), we evaluated whether AAMs are involved in the IL-25-mediated anticolitic effect.
Rizzo, A., Monteleone, I., Fina, D., Stolfi, C., Caruso, R., Fantini, M.c., et al. (2012). Inhibition of colitis by IL-25 associates with induction of alternatively activated macrophages. INFLAMMATORY BOWEL DISEASES, 18(3), 449-459 [10.1002/ibd.21799].
Inhibition of colitis by IL-25 associates with induction of alternatively activated macrophages
RIZZO, ANGELAMARIA;MONTELEONE, IVAN;FINA, DANIELE;STOLFI, CARMINE;CARUSO, ROBERTA;FANTINI, MASSIMO CLAUDIO;FRANZE', ELEONORA;PALLONE, FRANCESCO;MONTELEONE, GIOVANNI
2012-01-01
Abstract
Interleukin (IL)-25, a Th2-related factor, inhibits the synthesis of inflammatory cytokines by macrophages and attenuates experimental colitis in mice. The mechanism underlying the counterregulatory effect of IL-25, however, remains unknown. Since Th2-cytokines can abrogate inflammatory pathways by inducing alternatively activated macrophages (AAMs), we evaluated whether AAMs are involved in the IL-25-mediated anticolitic effect.| File | Dimensione | Formato | |
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