| First Author | Carter CR | Year | 2009 |
| Journal | Infect Immun | Volume | 77 |
| Issue | 12 | Pages | 5668-75 |
| PubMed ID | 19797068 | Mgi Jnum | J:155481 |
| Mgi Id | MGI:4414598 | Doi | 10.1128/IAI.00802-08 |
| Citation | Carter CR, et al. (2009) Complement receptor 3 deficiency influences lesion progression during Leishmania major infection in BALB/c mice. Infect Immun 77(12):5668-75 |
| abstractText | Leishmania major is an obligately intracellular protozoan parasite that causes cutaneous leishmaniasis. Like numerous intracellular pathogens, Leishmania exploits cell surface receptors as a means of entry into host cells. Complement receptor 3 (CR3; also called CD11b/CD18), a beta(2) integrin on phagocytic cells, is one such receptor. Ligation of CR3 has been shown to inhibit the production of interleukin-12, the cytokine that is pivotal in establishing the cell-mediated response necessary to combat intracellular infection. Here we investigate the role that CR3 plays in the establishment and progression of cutaneous leishmaniaisis in vivo. Dermal lesions of wild-type BALB/c mice are characteristically progressive and lead to extensive tissue necrosis coupled with elevated parasite burdens; CD11b-deficient BALB/c mice, however, demonstrate an intermediate phenotype characterized by chronic lesions and a reduced incidence of tissue damage. Infection followed by a reinfection challenge indicates that both susceptible (BALB/c) and resistant (C57BL/6) mice, regardless of CD11b status, develop resistance to L. major. In addition, CD11b does not bias the T helper cytokine response to L. major infection. Our results further indicate that CD11b is not necessary for disease resolution in resistant mice; rather, this protein appears to play a minor role in susceptibility. |
