Enhanced Toll-like receptor responses in the absence of signaling adaptor DAP12

被引:267
作者
Hamerman, JA
Tchao, NK
Lowell, CA
Lanier, LL [1 ]
机构
[1] Univ Calif San Francisco, Dept Microbiol & Immunol, San Francisco, CA 94143 USA
[2] Univ Calif San Francisco, Canc Res Inst, San Francisco, CA 94143 USA
[3] Univ Calif San Francisco, Dept Pulm & Crit Care Med, San Francisco, CA 94143 USA
[4] Univ Calif San Francisco, Dept Lab Med, San Francisco, CA 94143 USA
关键词
D O I
10.1038/ni1204
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
DAP12 is a signaling adaptor containing an immunoreceptor tyrosine-based activation motif (ITAM) that pairs with receptors on myeloid cells and natural killer cells. We examine here the responses of mice lacking DAP12 to stimulation through Toll-like receptors (TLRs). Unexpectedly, DAP12-deficient macrophages produced higher concentrations of inflammatory cytokines in response to a variety of pathogenic stimuli. Additionally, macrophages deficient in spleen tyrosine kinase (Syk), which signals downstream of DAP12, showed a phenotype identical to that of DAP12-deficient macrophages. DAP12-deficient mice were more susceptible to endotoxic shock and had enhanced resistance to infection by the intracellular bacterium Listeria monocytogenes. These data suggest that one or more DAP12-pairing receptors negatively regulate signaling through TLRs.
引用
收藏
页码:579 / 586
页数:8
相关论文
共 56 条
[1]   Toll-like receptor signalling [J].
Akira, S ;
Takeda, K .
NATURE REVIEWS IMMUNOLOGY, 2004, 4 (07) :499-511
[2]   DAP12-deficient mice fail to develop autoimmunity due to impaired antigen priming [J].
Bakker, ABH ;
Hoek, RM ;
Cerwenka, A ;
Blom, B ;
Lucian, L ;
McNeil, T ;
Murray, R ;
Phillips, JH ;
Sedgwick, JD ;
Lanier, LL .
IMMUNITY, 2000, 13 (03) :345-353
[3]   Myeloid DAP12-associating lectin (MDL)-1 is a cell surface receptor involved in the activation of myeloid cells [J].
Bakker, ABH ;
Baker, E ;
Sutherland, GR ;
Phillips, JH ;
Lanier, LL .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1999, 96 (17) :9792-9796
[4]   A role for triggering receptor expressed on myeloid cells-1 in host defense during the early-induced and adaptive phases of the immune response [J].
Bleharski, JR ;
Kiessler, V ;
Buonsanti, C ;
Sieling, PA ;
Stenger, S ;
Colonna, M ;
Modlin, RL .
JOURNAL OF IMMUNOLOGY, 2003, 170 (07) :3812-3818
[5]   The ubiquitin-modifying enzyme A20 is required for termination of Toll-like receptor responses [J].
Boone, DL ;
Turer, EE ;
Lee, EG ;
Ahmad, RC ;
Wheeler, MT ;
Tsui, C ;
Hurley, P ;
Chien, M ;
Chai, S ;
Hitotsumatsu, O ;
McNally, E ;
Pickart, C ;
Ma, A .
NATURE IMMUNOLOGY, 2004, 5 (10) :1052-1060
[6]   A DAP12-mediated pathway regulates expression of CC chemokine receptor 7 and maturation of human dendritic cells [J].
Bouchon, A ;
Hernández-Munain, C ;
Cella, M ;
Colonna, M .
JOURNAL OF EXPERIMENTAL MEDICINE, 2001, 194 (08) :1111-1122
[7]   Cutting edge: Inflammatory responses can be triggered by TREM-1, a novel receptor expressed on neutrophils and monocytes [J].
Bouchon, A ;
Dietrich, J ;
Colonna, M .
JOURNAL OF IMMUNOLOGY, 2000, 164 (10) :4991-4995
[8]   TREM-1 amplifies inflammation and is a crucial mediator of septic shock [J].
Bouchon, A ;
Facchetti, F ;
Weigand, MA ;
Colonna, M .
NATURE, 2001, 410 (6832) :1103-1107
[9]   ST2 is an inhibitor of interleukin 1 receptor and Toll-like receptor 4 signaling and maintains endotoxin tolerance [J].
Brint, EK ;
Xu, DM ;
Liu, HY ;
Dunne, A ;
McKenzie, ANJ ;
O'Neill, LAJ ;
Liew, FY .
NATURE IMMUNOLOGY, 2004, 5 (04) :373-379
[10]   Inhibition of interleukin 1 receptor/toll-like receptor signaling through the alternatively spliced, short form of MyD88 is due to its failure to recruit IRAK-4 [J].
Burns, K ;
Janssens, S ;
Brissoni, B ;
Olivos, N ;
Beyaert, R ;
Tschopp, J .
JOURNAL OF EXPERIMENTAL MEDICINE, 2003, 197 (02) :263-268