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Infection and Immunity, December 2009, p. 5668-5675, Vol. 77, No. 12
0019-9567/09/$08.00+0     doi:10.1128/IAI.00802-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

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

Cristina R. Carter, James P. Whitcomb, Jessica A. Campbell, Rami M. Mukbel, and Mary Ann McDowell*

Eck Institute for Global Health, Department of Biological Sciences, University of Notre Dame, Notre Dame, Indiana 46556

Received 27 June 2008/ Returned for modification 8 September 2008/ Accepted 14 September 2009

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.

* Corresponding author. Mailing address: Department of Biological Sciences, University of Notre Dame, 215 Galvin Life Science, Notre Dame, IN 46556. Phone: (574) 631-9771. Fax: (574) 631-7413. E-mail: mcdowell.11{at}nd.edu

{triangledown} Published ahead of print on 21 September 2009.

Editor: J. F. Urban, Jr.

Infection and Immunity, December 2009, p. 5668-5675, Vol. 77, No. 12
0019-9567/09/$08.00+0     doi:10.1128/IAI.00802-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.





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