| First Author | Takeda K | Year | 1999 |
| Journal | Immunity | Volume | 10 |
| Issue | 1 | Pages | 39-49 |
| PubMed ID | 10023769 | Mgi Jnum | J:53681 |
| Mgi Id | MGI:1333281 | Doi | 10.1016/s1074-7613(00)80005-9 |
| Citation | Takeda K, et al. (1999) Enhanced Th1 activity and development of chronic enterocolitis in mice devoid of Stat3 in macrophages and neutrophils. Immunity 10(1):39-49 |
| abstractText | We have generated mice with a cell type-specific disruption of the Stat3 gene in macrophages and neutrophils, The mutant mice are highly susceptible to endotoxin shock with increased production of inflammatory cytokines such as TNF alpha, IL-1, IFN gamma, and IL-6. Endotoxin-induced production of inflammatory cytokines is augmented because the suppressive effects of IL-10 on inflammatory cytokine production from macrophages and neutrophils are completely abolished. The mice show a polarized immune response toward the Th1 type and develop chronic enterocolitis with age. Taken together, Stat3 plays a critical role in deactivation of macrophages and neutrophils mainly exerted by IL-10. |
