Dendritic cell inhibitory and activating immunoreceptors (DCIR and DCAR) in duck: Genomic organization and expression

被引：5

作者：

Guo, Xiaoxin ^{[1
]}

Branton, William G. ^{[1
]}

Moon, Debra A. ^{[1
]}

Xia, Jianguo ^{[1
]}

MacDonald, Megan R. W. ^{[1
]}

Magor, Katharine E. ^{[1
]}

机构：

[1] Univ Alberta, Dept Biol Sci, Edmonton, AB T6G 2E9, Canada

来源：

MOLECULAR IMMUNOLOGY | 2008年 / 45卷 / 15期

基金：

加拿大自然科学与工程研究理事会;

关键词：

Mallard duck; Antigen presenting cells; DCIR lectin; C-type lectin immunoreceptors; Autoimmunity; ITIM; Comparative immunology/evolution;

D O I：

10.1016/j.molimm.2008.06.014

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

C-type lectin immunoreceptor genes encoding DC inhibitory and activating receptors (DCIR and DCAR) were identified in a spleen EST library of duck (Anas platyrhynchos). These receptors are of interest for their potential as regulators of antigen presenting cells. A genomic clone was isolated and fully sequenced, containing one DCIR gene and two DCAR genes arranged in tandem order. Duck DCIR encodes an inhibitory receptor that features an immunoreceptor tyrosine-based inhibitory motif (ITIM) in the cytoplasmic domain. DCAR1 is a pseudogene. DCAR2 encodes an activating receptor with a positively charged residue in the transmembrane region. Full-length and alternatively spliced forms of both DCIR and DCAR2 are apparent. Duck DCIR and DCAR transcripts are preferentially expressed in immune and mucosal tissues including spleen, bursa of Fabricius, intestine and lung. Targeting these receptors on dendritic cells holds potential for breaking tolerance or for enhancing immune responses, relevant to the duck model for hepatitis B and vaccination against avian influenza. (C) 2008 Elsevier Ltd. All rights reserved.

引用

页码：3942 / 3946

页数：5

共 23 条

[1]

Arce I, 2001, EUR J IMMUNOL, V31, P2733, DOI 10.1002/1521-4141(200109)31:9<2733::AID-IMMU2733>3.0.CO

[2]

2-X

[3]

Bates EEM, 1999, J IMMUNOL, V163, P1973

[4] BDCA2/FcεRlγ complex signals through a novel BCR-like pathway in human plasmacytoid dendritic cells [J].

Cao, Wei ;

Zhang, Li ;

Rosen, David B. ;

Bover, Laura ;

Watanabe, Gokuran ;

Bao, Musheng ;

Lanier, Lewis L. ;

Liu, Yong-Jun .

PLOS BIOLOGY, 2007, 5 (10) :2190-2200

[5] Differential antigen processing by dendritic cell subsets in vivo [J].

Dudziak, Diana ;

Kamphorst, Alice O. ;

Heidkamp, Gordon F. ;

Buchholz, Veit R. ;

Trumpfheller, Christine ;

Yamazaki, Sayuri ;

Cheong, Cheolho ;

Liu, Kang ;

Lee, Han-Woong ;

Park, Chae Gyu ;

Steinman, Ralph M. ;

Nussenzweig, Michel C. .

SCIENCE, 2007, 315 (5808) :107-111

[6] BDCA-2, a novel plasmacytoid dendritic cell-specific type IIC-type lectin, mediates antigen capture and is a potent inhibitor of interferon α/β induction [J].

Dzionek, A ;

Sohma, Y ;

Nagafune, J ;

Cella, M ;

Colonna, M ;

Facchetti, F ;

Günther, G ;

Johnston, I ;

Lanzavecchia, A ;

Nagasaka, T ;

Okada, T ;

Vermi, W ;

Winkels, G ;

Yamamoto, T ;

Zysk, M ;

Yamaguchi, Y ;

Schmitz, J .

JOURNAL OF EXPERIMENTAL MEDICINE, 2001, 194 (12) :1823-1834

[7] Cellular distribution of the C-type II lectin dendritic cell immunoreceptor (DCIR) and its expression in the rheumatic joint: identification of a subpopulation of DCIR plus T cells [J].

Eklow, C. ;

Makrygiannakis, D. ;

Backdahl, L. ;

Padyukov, L. ;

Ulfgren, A-K ;

Lorentzen, J. C. ;

Malmstrom, V. .

ANNALS OF THE RHEUMATIC DISEASES, 2008, 67 (12) :1742-1749

[8] Receptor cross-linking on human plasmacytoid dendritic cells leads to the regulation of IFN-α production [J].

Fanning, Stacey L. ;

George, Thaddeus C. ;

Feng, Di ;

Feldman, Steven B. ;

Megjugorac, Nicholas J. ;

Izaguirre, Alexander G. ;

Fitzgerald-Bocarsly, Patricia .

JOURNAL OF IMMUNOLOGY, 2006, 177 (09) :5829-5839

[9] Identification of lectin-like receptors expressed by antigen presenting cells and neutrophils and their mapping to a novel gene complex [J].

Flornes, LM ;

Bryceson, YT ;

Spurkland, A ;

Lorentzen, JC ;

Dissen, E ;

Fossum, S .

IMMUNOGENETICS, 2004, 56 (07) :506-517

[10] Dcir deficiency causes development of autoimmune diseases in mice due to excess expansion of dendritic cells [J].

Fujikado, Noriyuki ;

Saijo, Shinobu ;

Yonezawa, Tomo ;

Shimamori, Kazusuke ;

Ishii, Akina ;

Sugai, Sho ;

Kotaki, Hayato ;

Sudo, Katsuko ;

Nose, Masato ;

Iwakura, Yoichiro .

NATURE MEDICINE, 2008, 14 (02) :176-180

← 1 2 3 →