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Complement Receptor 3 Deficiency Influences Lesion Progression during Leishmania major Infection in BALB/c Mice

Carter, Cristina R., Whitcomb, James P., Campbell, Jessica A., Mukbel, Rami M., McDowell, Mary Ann
Infection and immunity 2009 v.77 no.12 pp. 5668-5675
CD4-positive T-lymphocytes, Leishmania major, cutaneous leishmaniasis, interleukin-12, macrophage-1 antigen, mice, necrosis, parasites, pathogens, phenotype, receptors
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 β₂ 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.