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High‐level expression of B7‐H1 molecules by dendritic cells suppresses the function of activated T cells and desensitizes allergen‐primed animals
Author(s) -
Kim Hee Kyung,
Guan Hongbing,
Zu Guorui,
Li Hui,
Wu Lizhi,
Feng Xu,
Elmets Craig,
Fu Yangxin,
Xu Hui
Publication year - 2006
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1189/jlb.0805436
Subject(s) - biology , microbiology and biotechnology , allergen , function (biology) , expression (computer science) , immunology , allergy , computer science , programming language
A body of evidence indicates that expression of the programmed cell death 1 (PD‐1) receptor by activated T cells plays an important role in the down‐regulation of immune responses; however, the functions of its known ligands, B7‐H1 (PD‐L1) and B7‐dendritic cell (DC; PD‐L2), at the effector phase of immune responses are less clear. In the current study, we investigated the roles of B7‐H1 in DC‐mediated regulation of hapten‐activated T cells and the delayed‐type contact hypersensitivity response in primed animals. We found that the expression of B7‐H1 and B7‐DC was induced on activation of DC by hapten stimulation. Blockade of B7‐H1, but not B7‐DC, enhanced the activity of hapten‐specific T cells. Interaction with a DC line that expresses high cell‐surface levels of B7‐H1 (B7‐H1/DC) suppressed the proliferation of, and cytokine production by, activated T cells. In vivo administration of hapten‐carrying B7‐H1/DC desensitized the response of sensitized animals to hapten challenge, and this desensitization was hapten‐specific. These data indicate that B7‐H1 expressed by DC mediates inhibitory signals for activated T cells and suppresses the elicitation of immune responses. The ability of B7‐H1/DC to inhibit the function of preactivated T cells in vivo suggests novel strategies for the treatment of immune response‐mediated disorders.