| First Author | Cotterell SE | Year | 1999 |
| Journal | Eur J Immunol | Volume | 29 |
| Issue | 1 | Pages | 203-14 |
| PubMed ID | 9933102 | Mgi Jnum | J:52285 |
| Mgi Id | MGI:1328724 | Doi | 10.1002/(SICI)1521-4141(199901)29:01<203::AID-IMMU203>3.0.CO;2-B |
| Citation | Cotterell SE, et al. (1999) Leishmania donovani infection initiates T cell-independent chemokine responses, which are subsequently amplified in a T cell-dependent manner. Eur J Immunol 29(1):203-14 |
| abstractText | Control of Leishmania donovani infection in immunocompetent mice is associated with hepatic inflammation and granuloma formation, both of which are absent in severe combined immunodeficient (scid) mice. In both BALB/c and scid mice, L. donovani infection induced a rapid hepatic accumulation of mRNA encoding macrophage inflammatory protein-1alpha (MIP-(1alpha), monocyte chemoattractant protein-1 (MCP-1) and interferon-gamma inducible protein-10 (gammaIP-10). This response was not preceded by increased IL-4 production in either strain, unlike that reported in other infectious disease models. Interestingly, only gammaIP-10 mRNA was maintained at elevated levels throughout the first 7 days of infection, by mechanisms involving CD4+ and CD8+ T cells, and CD4+CD8+ cells not activated in scid mice. By in vivo depletion and reconstitution of scid mice it was demonstrated that T cells regulate the expression of all three chemokines studied, while they themselves only produce gammaIP-10 in appreciable quantities. |
