Allergen-induced airway hyperreactivity is diminished in CD81-deficient mice

被引:39
作者
Deng, J
Yeung, VP
Tsitoura, D
DeKruyff, RH
Umetsu, DT
Levy, S
机构
[1] Stanford Univ, Med Ctr, Dept Med, Div Oncol, Stanford, CA 94305 USA
[2] Stanford Univ, Med Ctr, Dept Pediat, Div Immunol & Transplantat Biol, Stanford, CA 94305 USA
关键词
D O I
10.4049/jimmunol.165.9.5054
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
We demonstrated previously that CD81(-/-) mice have an impaired Th2 response. To determine whether this impairment affected allergen-induced airway hyperreactivity (AHR), CD81(-/-) BALB/c mice and CD81(+/+) littermates were sensitized i.p. and challenged intranasally with OVA, Although wild type developed severe AHR, CD81(-/-) mice showed normal airway reactivity and reduced airway inflammation. Nevertheless, OVA-specific T cell proliferation was similar in both groups of mice, Analysis of cytokines secreted by the responding CD81(-/-) T cells, particularly those derived from peribronchial draining lymph nodes, revealed a dramatic reduction in IL-4, IL-5, and IL-13 synthesis. The decrease in cytokine production was not due to an intrinsic T cell deficiency because naive CD81(-/-) T cells responded to polyclonal Th1 and Th2 stimulation with normal proliferation and cytokine production. Moreover, there was an increase in T cells and a decrease in B cells in peribronchial lymph nodes and in spleens of immunized CD81(-/-) mice compared with wild-type animals. Interestingly OVA-specific Ig levels, including IgE, were similar in CD81(-/-) and CD81(+/+) mice. Thus, CD81 plays a role in the development of AHR not by influencing Ag-specific IgE production but by regulating local cytokine production.
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页码:5054 / 5061
页数:8
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共 52 条
  • [1] Abrogation of bronchial eosinophilic inflammation and airway hyperreactivity in signal transducers and activators of transcription (STAT)6-deficient mice
    Akimoto, T
    Numata, F
    Tamura, M
    Takata, Y
    Higashida, N
    Takashi, T
    Takeda, K
    Akira, S
    [J]. JOURNAL OF EXPERIMENTAL MEDICINE, 1998, 187 (09) : 1537 - 1542
  • [2] BOCHNER BS, 1994, ANNU REV IMMUNOL, V12, P295
  • [3] BRADBURY LE, 1992, J IMMUNOL, V149, P2841
  • [4] ATTENUATION OF ALLERGIC AIRWAY INFLAMMATION IN IL-4 DEFICIENT MICE
    BRUSSELLE, GG
    KIPS, JC
    TAVERNIER, JH
    VANDERHEYDEN, JG
    CUVELIER, CA
    PAUWELS, RA
    BLUETHMANN, H
    [J]. CLINICAL AND EXPERIMENTAL ALLERGY, 1994, 24 (01) : 73 - 80
  • [5] ASSOCIATION OF ASTHMA WITH SERUM IGE LEVELS AND SKIN-TEST REACTIVITY TO ALLERGENS
    BURROWS, B
    MARTINEZ, FD
    HALONEN, M
    BARBEE, RA
    CLINE, MG
    [J]. NEW ENGLAND JOURNAL OF MEDICINE, 1989, 320 (05) : 271 - 277
  • [6] Cohn L, 1998, J IMMUNOL, V161, P3813
  • [7] Interleukin 4, but not interleukin 5 or eosinophils, is required in a murine model of acute airway hyperreactivity
    Corry, DB
    Folkesson, HG
    Warnock, ML
    Erle, DJ
    Matthay, MA
    WienerKronish, JP
    Locksley, RM
    [J]. JOURNAL OF EXPERIMENTAL MEDICINE, 1996, 183 (01) : 109 - 117
  • [8] Corry DB, 1997, J EXP MED, V185, P1715
  • [9] Dabbagh K, 1999, J IMMUNOL, V162, P6233
  • [10] ACTIVATION OF HUMAN EOSINOPHIL AND NEUTROPHIL FUNCTIONS BY HEMATOPOIETIC GROWTH-FACTORS - COMPARISONS OF IL-1, IL-3, IL-5 AND GM-CSF
    FABIAN, I
    KLETTER, Y
    MOR, S
    GELLERBERNSTEIN, C
    BENYAAKOV, M
    VOLOVITZ, B
    GOLDE, DW
    [J]. BRITISH JOURNAL OF HAEMATOLOGY, 1992, 80 (02) : 137 - 143