IL-4 INDUCES CHEMOTAXIS OF BLOOD EOSINOPHILS FROM ATOPIC-DERMATITIS PATIENTS, BUT NOT FROM NORMAL INDIVIDUALS

被引:47
作者
DUBOIS, GR
BRUIJNZEELKOOMEN, CAFM
BRUIJNZEEL, PLB
机构
[1] TNO,DEPT PHARMACOL,MED BIOL LAB,2288 GJ RIJSWIJK,NETHERLANDS
[2] UNIV UTRECHT HOSP,DEPT DERMATOL ALLERGOL,UTRECHT,NETHERLANDS
[3] SWISS INST ALLERGY & ASTHMA RES,DAVOS,SWITZERLAND
关键词
ATOPIC DERMATITIS; CYTOKINES; EOSINOPHILS; MIGRATION; INTERLEUKIN; 4;
D O I
10.1111/1523-1747.ep12382362
中图分类号
R75 [皮肤病学与性病学];
学科分类号
100206 ;
摘要
T lymphocytes present in allergically inflamed tissue synthesize and secrete the cytokines interleukin (IL)-3, IL-4, IL-5, and granulocyte/macrophage colony-stimulating factor (GM-CSF). IL-3, IL-5, and GM-CSF, but also IL-4, may act as a chemotaxin on eosinophils. In contrast to the former cytokines, IL-4 is only chemotactic for eosinophils from the peripheral blood of patients with atopic dermatitis and not for eosinophils from normal individuals. IL-4 has the same chemotactic potency as the other cytokines. The optimal chemotactic potency is reached at a concentration of 10 nM. In contrast, neutrophils do not respond chemotactically to IL-4. Checkerboard analysis, inhibition studies with monoclonal anti-IL-4 antibodies, and desensitization experiments indicated specific interaction of IL-4 with eosinophils. In eosinophils from normal individuals, IL-4 responsiveness could be induced by pretreatment of the cells with IL-5 and GM-CSF. In addition to the fact that IL-4 may be responsible for selective eosinophil transendothelial migration, IL-4 may exert an important modulatory mode of action on eosinophil migration and function within allergically inflamed tissue. Our findings suggest the presence of a functional IL-4R on eosinophils from atopic dermatitis patients.
引用
收藏
页码:843 / 846
页数:4
相关论文
共 23 条
  • [1] EOSINOPHIL MIGRATION IN ATOPIC DERMATITIS-I - INCREASED MIGRATORY RESPONSES TO N-FORMYL-METHIONYL-LEUCYL-PHENYLALANINE, NEUTROPHIL-ACTIVATING FACTOR, PLATELET-ACTIVATING-FACTOR, AND PLATELET FACTOR-IV
    BRUIJNZEEL, PLB
    KUIJPER, PHM
    RIHS, S
    BETZ, S
    WARRINGA, RAJ
    KOENDERMAN, L
    [J]. JOURNAL OF INVESTIGATIVE DERMATOLOGY, 1993, 100 (02) : 137 - 142
  • [2] BRUIJNZEELKOOME.C, 1988, BRIT J DERMATOL, V118, P229
  • [3] BRUIJNZEELKOOMEN C, 1990, ALLERGOLOGIE, V13, P325
  • [4] HUMAN RECOMBINANT INTERLEUKIN-4 INDUCES FC-EPSILON RECEPTORS (CD23) ON NORMAL HUMAN LYMPHOCYTES-B
    DEFRANCE, T
    AUBRY, JP
    ROUSSET, F
    VANBERVLIET, B
    BONNEFOY, JY
    ARAI, N
    TAKEBE, Y
    YOKOTA, T
    LEE, F
    ARAI, K
    DEVRIES, J
    BANCHEREAU, J
    [J]. JOURNAL OF EXPERIMENTAL MEDICINE, 1987, 165 (06) : 1459 - 1467
  • [5] HANIFIN JM, 1980, ACTA DERM-VENEREOL, V92, P44, DOI [DOI 10.2340/00015555924447, 10.2340/00015555924447]
  • [6] IDENTIFICATION OF A T-CELL-DERIVED B-CELL GROWTH-FACTOR DISTINCT FROM INTERLEUKIN-2
    HOWARD, M
    FARRAR, J
    HILFIKER, M
    JOHNSON, B
    TAKATSU, K
    HAMAOKA, T
    PAUL, WE
    [J]. JOURNAL OF EXPERIMENTAL MEDICINE, 1982, 155 (03) : 914 - 923
  • [7] MURINE B-CELL STIMULATORY FACTOR-I (INTERLEUKIN-4) INCREASES EXPRESSION OF THE FC RECEPTOR FOR IGE ON MOUSE B-CELLS
    HUDAK, SA
    GOLLNICK, SO
    CONRAD, DH
    KEHRY, MR
    [J]. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1987, 84 (13) : 4606 - 4610
  • [8] LAWAHAMI Y, 1988, J EXP MED, V168, P85
  • [9] LEIFERMAN K, 1985, NEW ENGL J MED, V313, P47
  • [10] MOSER R, 1992, J IMMUNOL, V149, P1432