The role of TARC in the pathogenesis of allergic asthma

被引:21
作者
Berin, MC [1 ]
机构
[1] CUNY Mt Sinai Sch Med, Div Pediat Allergy & Immunol, New York, NY 10029 USA
关键词
D O I
10.1358/dnp.2002.15.1.660501
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
TARC (thymus and activation-regulated chemokine), as a selective chemoattractant of Th2 cells, is a reasonable candidate as a key regulator of Th2-mediated inflammation in allergic asthma. Studies have determined that TARC is up-regulated in the airways of human subjects with asthma and that CCR4- and CCR8-bearing T cells are also present in the airways of asthmatic subjects after allergen challenge. Mouse models of allergic airway inflammation have shown that neutralization of TARC can not only inhibit T-cell and eosinophil infiltration into the lung but can also inhibit bronchial hyperresponsiveness. The exact mechanism by which TARC can participate in allergic inflammation and what triggers the expression of TARC following allergen exposure is still unknown. Studies suggest that it could be involved not only in allergic asthma, but in the pathogenesis of allergic Th2-mediated diseases in general. (C) 2002 Prous Science. All rights reserved.
引用
收藏
页码:10 / 16
页数:7
相关论文
共 62 条
[1]  
Andrew DP, 1998, J IMMUNOL, V161, P5027
[2]   Regulated production of the T helper 2-type T-cell chemoattractant TARC by human bronchial epithelial cells in vitro and in human lung xenografts [J].
Berin, MC ;
Eckmann, L ;
Broide, DH ;
Kagnoff, MF .
AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY, 2001, 24 (04) :382-389
[3]  
Bernardini G, 1998, EUR J IMMUNOL, V28, P582, DOI 10.1002/(SICI)1521-4141(199802)28:02<582::AID-IMMU582>3.0.CO
[4]  
2-A
[5]   Differential expression of chemokine receptors and chemotactic responsiveness of type 1 T helper cells (Th1s) and Th2s [J].
Bonecchi, R ;
Bianchi, G ;
Bordignon, PP ;
D'Ambrosio, D ;
Lang, R ;
Borsatti, A ;
Sozzani, S ;
Allavena, P ;
Gray, PA ;
Mantovani, A ;
Sinigaglia, F .
JOURNAL OF EXPERIMENTAL MEDICINE, 1998, 187 (01) :129-134
[6]   EOSINOPHILIC INFLAMMATION IN ASTHMA [J].
BOUSQUET, J ;
CHANEZ, P ;
LACOSTE, JY ;
BARNEON, G ;
GHAVANIAN, N ;
ENANDER, I ;
VENGE, P ;
AHLSTEDT, S ;
SIMONYLAFONTAINE, J ;
GODARD, P ;
MICHEL, FB .
NEW ENGLAND JOURNAL OF MEDICINE, 1990, 323 (15) :1033-1039
[7]   EOSINOPHILS, T-LYMPHOCYTES, MAST-CELLS, NEUTROPHILS, AND MACROPHAGES IN BRONCHIAL BIOPSY SPECIMENS FROM ATOPIC SUBJECTS WITH ASTHMA - COMPARISON WITH BIOPSY SPECIMENS FROM ATOPIC SUBJECTS WITHOUT ASTHMA AND NORMAL CONTROL SUBJECTS AND RELATIONSHIP TO BRONCHIAL HYPERRESPONSIVENESS [J].
BRADLEY, BL ;
AZZAWI, M ;
JACOBSON, M ;
ASSOUFI, B ;
COLLINS, JV ;
IRANI, AMA ;
SCHWARTZ, LB ;
DURHAM, SR ;
JEFFERY, PK ;
KAY, AB .
JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY, 1991, 88 (04) :661-674
[8]   ALLERGEN-INDUCED AIRWAY INFLAMMATION AND BRONCHIAL RESPONSIVENESS IN WILD-TYPE AND INTERLEUKIN-4-DEFICIENT MICE [J].
BRUSSELLE, G ;
KIPS, J ;
JOOS, G ;
BLUETHMANN, H ;
PAUWELS, R .
AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY, 1995, 12 (03) :254-259
[9]   Aberrant in vivo T helper type 2 cell response and impaired eosinophil recruitment in CC chemokine receptor 8 knockout mice [J].
Chensue, SW ;
Lukacs, NW ;
Yang, TY ;
Shang, XZ ;
Frait, KA ;
Kunkel, SL ;
Kung, T ;
Wiekowski, MT ;
Hedrick, JA ;
Cook, DN ;
Zingoni, A ;
Narula, SK ;
Zlotnik, A ;
Barrat, FJ ;
O'Garra, A ;
Napolitano, M ;
Lira, SA .
JOURNAL OF EXPERIMENTAL MEDICINE, 2001, 193 (05) :573-584
[10]   A key role for CC chemokine receptor 4 in lipopolysaccharide-induced endotoxic shock [J].
Chvatchko, Y ;
Hoogewerf, AJ ;
Meyer, A ;
Alouani, S ;
Juillard, P ;
Buser, R ;
Conquet, F ;
Proudfoot, AEI ;
Wells, TNC ;
Power, CA .
JOURNAL OF EXPERIMENTAL MEDICINE, 2000, 191 (10) :1755-1763