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Published online before print September 14, 2006

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(Journal of Leukocyte Biology. 2006;80:1251-1261.)
© 2006 by Society for Leukocyte Biology

Effects of LPS-mediated bystander activation in the innate immune system

Department of Immunology, University of Connecticut Health Center, Farmington, Connecticut, USA

¹ Correspondence: Department of Immunology, University of Connecticut Health Center, 263 Farmington Ave., MC1319, Farmington, CT 06030, USA. E-mail: vella{at}uchc.edu

ABSTRACT

LPS induces dendritic cell (DC) activation, but the precise in vivo mechanism is unclear since DCs express low levels of TLR4. Here, it is shown that DCs can be activated in response to LPS through a bystander mechanism. This result was obtained using chimeric mice reconstituted with LPS-responsive and nonresponsive bone marrow cells. Thus, after indirect in vivo conditioning by LPS, bystander-activated DCs (LPS nonresponsive) up-regulated CD86. This up-regulation occurred even when LPS-responsive cells were MyD88 deficient. Functional analysis demonstrated that in vivo LPS conditioning endowed both the LPS-responsive and bystander cells with the ability to produce IFN- in response to TLR9 stimulation in vitro. IFN- production was also shown to be important for enhanced T-bet gene expression but not important for up-regulation of CD86. To investigate aspects of the mechanism, we used intracellular cytokine staining and found that NKDCs were responsible for at least some of the IFN- production. Thus, our in vivo results demonstrated that bacterial LPS can bridge activation of various cellular populations of the innate immune system through a bystander mechanism.

Key Words: dendritic cells • cytokines

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