| First Author | Rosas LE | Year | 2005 |
| Journal | Eur J Immunol | Volume | 35 |
| Issue | 2 | Pages | 515-23 |
| PubMed ID | 15668916 | Mgi Jnum | J:95617 |
| Mgi Id | MGI:3526632 | Doi | 10.1002/eji.200425422 |
| Citation | Rosas LE, et al. (2005) CXCR3(-/-) mice mount an efficient Th1 response but fail to control Leishmania major infection. Eur J Immunol 35(2):515-23 |
| abstractText | Chemokines play a critical role in recruitment of leukocytes to the site of infection, which is essential for host defense. We analyzed the role of CXC chemokine receptor 3 (CXCR3) in the control of cutaneous leishmaniasis using CXCR3(-/-) C57BL/6 mice. We found that Leishmania major-infected CXCR3(-/-) mice mount an efficient Th1 response as evident by markedly increased serum levels of Th1-associated IgG2a and significant production of IFN-gamma and IL-12 by the draining lymph node cells, restrict systemic spread of infection, but fail to control parasite replication at the site of infection and develop chronic non-healing lesions. Furthermore, the inability of CXCR3(-/-) mice to control cutaneous L. major growth was associated with fewer CD4(+) and CD8(+) T cells and significantly lower levels of IFN-gamma in their lesions as compared to CXCR3(+/+) mice. These results demonstrate that CXCR3 plays a critical role in the host defense against cutaneous leishmaniasis caused by L. major. Furthermore, they also suggest that the susceptibility of CXCR3(-/-) mice to L. major is due to impaired CD4(+) and CD8(+) T cell trafficking and decreased production of IFN-gamma at the site of infection rather than to their inability to mount a parasite-specific Th1 response. |
