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A reduced population of CD103(+)CD11b(+) dendritic cells has a limited impact on oral Salmonella infection.

Abstract：

:CD103(+)CD11b(+) dendritic cells (DC) are the major migratory DC subset in the small intestine lamina propria (siLP) and their survival is dependent on the transcription factor interferon regulatory factor 4 (IRF4). Mice with a DC-specific deletion of irf4 (CD11c-cre.Irf4 mice) have reduced mucosal CD103(+)CD11b(+) DC and altered T cell differentiation to protein antigen. The influence of CD103(+)CD11b(+) DC on oral infection with the gastrointestinal pathogen Salmonella, however, is poorly understood and is investigated here. We show that, despite being infected with Salmonella, CD11c-cre.Irf4 mice (called Cre(+) mice) conserve the reduction in CD103(+)CD11b(+) DC observed in naive Cre(+) mice, particularly in the mesenteric lymph nodes (MLN) but also in the siLP at day 3 post infection. Moreover, Salmonella-infected Cre(+) mice have a similar bacterial burden in intestinal tissues (siLP, MLN and Peyer's patches) as well as the spleen compared to infected Cre(-) controls. The T cell compartment, including the frequency of IFN-γ and IL-17-producing T cells, is not altered in intestinal tissues of Salmonella-infected Cre(+) mice relative to infected Cre(-) controls. In addition, no difference between infected Cre(+) and Cre(-) mice was observed in either the concentration of IL-6 or IL-17 in whole tissue lysates of siLP, MLN or Peyer's patches or in the serum concentration of Salmonella-specific IgG and IgM. Overall the data suggest that the reduction of CD103(+)CD11b(+) DC in Cre(+) mice has little if any impact on Salmonella burden in infected tissues or eliciting effector functions important in host survival at later stages of the infection.

journal_name

Immunol Lett

journal_title

Immunology letters

authors

Fernández-Santoscoy M,Wenzel UA,Persson E,Yrlid U,Agace W,Wick MJ

doi

10.1016/j.imlet.2016.05.012

subject

Has Abstract

pub_date

2016-08-01 00:00:00

pages

72-80

eissn

0165-2478

issn

1879-0542

pii

S0165-2478(16)30088-8

journal_volume

176

pub_type

杂志文章

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