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Blood, 15 April 2007, Vol. 109, No. 8, pp. 3308-3315.
Prepublished online as a Blood First Edition Paper on December 14, 2006; DOI 10.1182/blood-2006-08-040337.
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Submitted August 9, 2006
Accepted December 8, 2006
TLR agonists induce regulatory dendritic cells to recruit Th1 cells via preferential IP-10 secretion and inhibit Th1 proliferation
Cheng Qian, Huazhang An, Yizhi Yu, Shuxun Liu, and Xuetao Cao*
Institute of Immunology, & National Key Laboratory of Medical Immunology, Second Military Medical University, Shanghai, China
* Corresponding author; email: caoxt{at}public3.sta.net.cn.
Dendritic cells (DCs) and chemokines are important mediators linking innate and adaptive immunity upon activation by Toll-like receptor (TLR) agonists. We previously identified a kind of regulatory DC subset (diffDCs) which differentiated from mature DCs under splenic stroma and inhibit T cell proliferation. What's responsiveness of such regulatory DCs to TLR agonists and their pattern of chemokine production remain to be determined. Here, we report that the regulatory DCs secrete higher level of CXCR3 chemokine IFN- -induced protein-10 (IP-10) than immature DCs (imDCs), and more IP-10 is produced after stimulation with TLR 2, 4, 3, 9 ligands. Blockade of IFN- / inhibits IP-10 production by TLR agonists-activated regulatory DCs. We show that the increased IRF-3 and IFN--induced STAT1 activation are responsible for the autocrine IFN--dependent preferential production of IP-10 by regulatory DCs. In addition, stimulation with recombinant mouse IFN-/ induces more IP-10 production in regulatory DCs than that in imDCs. Moreover, the regulatory DCs selectively recruit more Th1 cells through IP-10 and inhibit Th1 proliferation. Our results demonstrate a new manner for regulatory DCs to downregulate T cell response by preferential IP-10 production and inhibition of recruited Th1 cell proliferation.
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