Enhanced antibacterial potential in UBP43-deficient mice against Salmonella typhimurium infection by up-regulating type I IFN signaling
- Authors
- Kim K.I.; Malakhova O.A.; Hoebe K.; Yan M.; Beutler B.; Zhang D.-E.
- Issue Date
- Jul-2005
- Publisher
- American Association of Immunologists
- Citation
- Journal of Immunology, v.175, no.2, pp 847 - 854
- Pages
- 8
- Journal Title
- Journal of Immunology
- Volume
- 175
- Number
- 2
- Start Page
- 847
- End Page
- 854
- URI
- https://scholarworks.sookmyung.ac.kr/handle/2020.sw.sookmyung/15762
- DOI
- 10.4049/jimmunol.175.2.847
- ISSN
- 0022-1767
1550-6606
- Abstract
- ISG15 is an IFN-inducible ubiquitin-like protein and its expression and conjugation to target proteins are dramatically induced upon viral or bacterial infection. We have generated a UBP43 knockout mouse model that is lacking an ISG15-specific isopeptidase to study the biological role of the protein ISGylation system. We report that UBP43-deficient mice are hypersensitive to LPS-induced lethality and that TIR domain-containing adapter inducing IFN-β → IFN regulatory factor 3 → type I IFN is the major axis to induce protein ISGylation and UBP43 expression in macrophages upon LPS treatment. In ubp43-/- macrophages, upon LPS treatment we detected increased expression of IFN-stimulated genes, including genes for several cytokines and chemokines involved in the innate immune response. The ubp43-/- mice were able to restrict the growth of Salmonella typhimurium more efficiently than wild-type mice. These results clearly demonstrate two aspects of IFN-signaling, a beneficial effect against pathogens but a detriment to the body without strict control. Copyright © 2005 by The American Association of Immunologists, Inc.
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