Chemokines and chemokine receptors: Their role in allergic airway disease

被引:68
作者
Rothenberg, ME
Zimmermann, N
Mishra, A
Brandt, E
Birkenberger, LA
Hogan, SP
Foster, PS
机构
[1] Childrens Hosp, Ctr Med, Dept Pediat, Div Pulm Med Allergy & Clin Immunol, Cincinnati, OH 45229 USA
[2] Australian Natl Univ, John Curtin Sch Med Res, Div Biochem & Mol Biol, Canberra, ACT 0200, Australia
[3] Hoechst Mar Roussel, Bridgewater, NJ 08807 USA
关键词
chemokines; asthma; allergy; eotaxin; eosinophils;
D O I
10.1023/A:1020531322556
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
One of the hallmarks of allergic pulmonary disorders is the accumulation of an abnormally large number of leukocytes including eosinophils, neutrophils, lymphocytes, basophils, and macrophages in the lung (1). There is now substantial evidence that eosinophils, under the control of T lymphocytes, are major effector cells in the pathogenesis of asthma. Therefore, understanding the mechanisms by which eosinophils accumulate and are activated in tissues is a fundamental question very relevant to allergic diseases. Another characteristic of allergic inflammation is the activation of leukocytes resulting in the release of biologically active mediators, such as histamine from mast cells and basophils. It is now apparent that chemokines are patent leukocyte chemoattractants, cellular activating factors, histamine releasing factors, and regulators of homeostatic immunity making them particularly important in the pathogenesis of airway inflammation in asthma (2). In this regard, chemokines are attractive new therapeutic targets for the treatment of allergic disease. This article focuses on recently emerging data on the importance of chemokines and their receptors in allergic airway inflammation.
引用
收藏
页码:250 / 265
页数:16
相关论文
共 131 条
[21]   REQUIREMENT OF MIP-1-ALPHA FOR AN INFLAMMATORY RESPONSE TO VIRAL-INFECTION [J].
COOK, DN ;
BECK, MA ;
COFFMAN, TM ;
KIRBY, SL ;
SHERIDAN, JF ;
PRAGNELL, IB ;
SMITHIES, O .
SCIENCE, 1995, 269 (5230) :1583-1585
[22]   Epithelial cells are a major cellular source of the chemokine eotaxin in the guinea pig lung [J].
Cook, EB ;
Stahl, JL ;
Lilly, CM ;
Haley, KJ ;
Sanchez, H ;
Luster, AD ;
Graziano, FM ;
Rothenberg, ME .
ALLERGY AND ASTHMA PROCEEDINGS, 1998, 19 (01) :15-22
[23]   Interleukin 4, but not interleukin 5 or eosinophils, is required in a murine model of acute airway hyperreactivity [J].
Corry, DB ;
Folkesson, HG ;
Warnock, ML ;
Erle, DJ ;
Matthay, MA ;
WienerKronish, JP ;
Locksley, RM .
JOURNAL OF EXPERIMENTAL MEDICINE, 1996, 183 (01) :109-117
[24]   MONOCYTE CHEMOTACTIC PROTEIN-3 IS A MOST EFFECTIVE BASOPHIL-ACTIVATING AND EOSINOPHIL-ACTIVATING CHEMOKINE [J].
DAHINDEN, CA ;
GEISER, T ;
BRUNNER, T ;
VONTSCHARNER, V ;
CAPUT, D ;
FERRARA, P ;
MINTY, A ;
BAGGIOLINI, M .
JOURNAL OF EXPERIMENTAL MEDICINE, 1994, 179 (02) :751-756
[25]   The beta-chemokine receptor genes CCR1 (CMKBR1), CCR2 (CMKBR2), and CCR3 (CMKBR3) cluster within 285 kb on human chromosome 3p21 [J].
Daugherty, BL ;
Springer, MS .
GENOMICS, 1997, 41 (02) :294-295
[26]   Cloning, expression, and characterization of the human eosinophil eotaxin receptor [J].
Daugherty, BL ;
Siciliano, SJ ;
DeMartino, JA ;
Malkowitz, L ;
Sirotina, A ;
Springer, MS .
JOURNAL OF EXPERIMENTAL MEDICINE, 1996, 183 (05) :2349-2354
[27]   Genetic restriction of HIV-1 infection and progression to AIDS by a deletion allele of the CKR5 structural gene [J].
Dean, M ;
Carrington, M ;
Winkler, C ;
Huttley, GA ;
Smith, MW ;
Allikmets, R ;
Goedert, JJ ;
Buchbinder, SP ;
Vittinghoff, E ;
Gomperts, E ;
Donfield, S ;
Vlahov, D ;
Kaslow, R ;
Saah, A ;
Rinaldo, C ;
Detels, R ;
OBrien, SJ .
SCIENCE, 1996, 273 (5283) :1856-1862
[28]   Sorting out the cytokines of asthma [J].
Drazen, JM ;
Arm, JP ;
Austen, KF .
JOURNAL OF EXPERIMENTAL MEDICINE, 1996, 183 (01) :1-5
[29]   DEVELOPMENT OF A PROLONGED EOSINOPHIL-RICH INFLAMMATORY LEUKOCYTE INFILTRATION IN THE GUINEA-PIG ASTHMATIC RESPONSE TO OVALBUMIN INHALATION [J].
DUNN, CJ ;
ELLIOTT, GA ;
OOSTVEEN, JA ;
RICHARDS, IM .
AMERICAN REVIEW OF RESPIRATORY DISEASE, 1988, 137 (03) :541-547
[30]   The CC chemokine antagonist Met-RANTES inhibits eosinophil effector functions through the chemokine receptors CCR1 and CCR3 [J].
Elsner, J ;
Petering, H ;
Hochstetter, R ;
Kimmig, D ;
Wells, TNC ;
Kapp, A ;
Proudfoot, AEJ .
EUROPEAN JOURNAL OF IMMUNOLOGY, 1997, 27 (11) :2892-2898