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Immunol Lett. 2014 Mar-Apr;158(1-2):42-51. doi: 10.1016/j.imlet.2013.11.015. Epub 2013 Dec 1.

Dendritic cells play a role in host susceptibility to Cryptosporidium parvum infection.

Author information

1
Atlanta VA Medical Center, Decatur, GA 30033, United States; Department of Pediatrics, Emory University, Atlanta, GA 30322, United States.
2
Department of Pediatrics, Emory University, Atlanta, GA 30322, United States.
3
Atlanta VA Medical Center, Decatur, GA 30033, United States; Department of Pediatrics, Emory University, Atlanta, GA 30322, United States. Electronic address: jmead@emory.edu.

Abstract

Our previous studies have described dendritic cells (DCs) to be important sources of Th1 cytokines such as IL-12 and IL-2 in vitro, following stimulation with Cryptosporidium parvum antigens. We further established the role of DCs during cryptosporidiosis using a diphtheria toxin promoter regulated transgenic CD11c-DTR/EGFP mouse model. In vivo depletion of CD11c(+) cells in CD11c-DTR-Tg mice significantly increased susceptibility to C. parvum infection. Adoptive transfer of unstimulated or antigen stimulated DCs into CD11c(+) depleted CD11c-DTR-Tg mice resulted in an early decrease in parasite load at 4 days post infection. However, this response was transient since parasite load increased in mice engrafted with either unstimulated DCs or DCs stimulated with solubilized antigen by 6 days post infection. In contrast, in mice engrafted with DCs stimulated with live sporozoites, parasite load remained low during the entire period, suggesting the development of a more effective and sustained response. A corresponding increase in IFN-γ expression in T cells from spleen and mesenteric lymph nodes was also noted. Consistent with the in vivo engraftment study, DCs that are pulsed with live sporozoites in vitro and co-cultured with CD4(+) and CD8(+) T cells produced higher IFN-γ levels. Our study establishes the importance of DCs in susceptibility to infection by C. parvum and as important mediators of immune responses.

KEYWORDS:

CD11c-DTR-Tg; Cryptosporidium; Dendritic cells; Innate response

PMID:
24295591
DOI:
10.1016/j.imlet.2013.11.015
[Indexed for MEDLINE]

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