| First Author | Singh UP | Year | 2003 |
| Journal | J Immunol | Volume | 171 |
| Issue | 3 | Pages | 1401-6 |
| PubMed ID | 12874231 | Mgi Jnum | J:84654 |
| Mgi Id | MGI:2668791 | Doi | 10.4049/jimmunol.171.3.1401 |
| Citation | Singh UP, et al. (2003) Inhibition of IFN-gamma-inducible protein-10 abrogates colitis in IL-10(-/-) mice. J Immunol 171(3):1401-6 |
| abstractText | A deficiency in understanding the steps responsible for colitis is the lack of comprehension for the role chemokines play in mucosal inflammation. IFN-gamma-inducible protein-10 (IP-10) and CXCR3 are highly expressed at sites of colitis. Our findings show that IP-10 significantly contributes to the development of Th1 and inflammatory responses. Specifically, IP-10 inhibition in IL-10(-/-) mice attenuates the associated increases in serum and/or local amyloid A, IL-2, IL-6, TNF-alpha, IFN-gamma, IL-1alpha, and IL-1beta with colitis as compared with IL-10(-/-) mice that develop colitis similar to human Crohn's disease. Correspondingly, the rate or intensity of inflammation in IL-10(-/-) mice treated with anti-IP-10 Abs showed improved scoring of inflammation, compared with control IL-10(-/-) mice. This study provides important and novel information regarding IP-10 as a target for the treatment of colitis. |
