Dendritic cells are associated with augmentation of antigen sensitization by influenza A virus infection in mice

被引:4
作者
Yamamoto, N
Suzuki, S
Shirai, A
Suzuki, M
Nakazawa, M
Nagashima, Y
Okubo, T
机构
[1] Yokohama City Univ, Sch Med, Dept Internal Med 1, Yokohama, Kanagawa 232, Japan
[2] Yokohama City Univ, Sch Med, Dept Parasitol, Yokohama, Kanagawa 232, Japan
[3] Yokohama City Univ, Sch Med, Dept Pathol, Yokohama, Kanagawa 232, Japan
关键词
allergy; dendritic cell; virus infection; MHC class II; sensitization;
D O I
10.1002/1521-4141(200001)30:1<316::AID-IMMU316>3.0.CO;2-0
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 [免疫学];
摘要
To study the mechanisms responsible for enhanced sensitization of inhaled antigen in respiratory viral infections, we examined the contribution of dendritic cells (DC) and T lymphocytes to the development of inhalation sensitization during infection with influenza A virus in mice. BALB/c mice were sensitized by inhalation of ovalbumin (OA) from 3 to 7 days after the inoculation with influenza A virus, and were challenged with OA 3 weeks later. Airway responsiveness and serum OA-specific IgE were increased. The numbers of eosinophils and CD4(+) and CD8(+) T cells in bronchoalveolar ravage fluid were also increased. These changes were not observed in animals only sensitized with OA or only inoculated with the virus. In animals only inoculated with the virus, DC were immunohistochemically detected on the bronchial epithelium on days 2-5. With OA inhalation after virus inoculation, DC with high expression of MHC class II were retained for 5 weeks. These results show that influenza virus infection induces the migration of DC to the bronchial epithelium, and that simultaneous inhalation of antigen causes the loading of antigen-peptide/class II molecule complex on DC. Thus, the migration of DC in viral infection may play some role in the augmentation of antigen sensitization.
引用
收藏
页码:316 / 326
页数:11
相关论文
共 41 条
[1]
Dendritic cells and the control of immunity [J].
Banchereau, J ;
Steinman, RM .
NATURE, 1998, 392 (6673) :245-252
[2]
INFLUENZA VIRUS-INFECTED DENDRITIC CELLS STIMULATE STRONG PROLIFERATIVE AND CYTOLYTIC RESPONSES FROM HUMAN CD8+ T-CELLS [J].
BHARDWAJ, N ;
BENDER, A ;
GONZALEZ, N ;
BUI, LK ;
GARRETT, MC ;
STEINMAN, RM .
JOURNAL OF CLINICAL INVESTIGATION, 1994, 94 (02) :797-807
[3]
Lung inflammation and epithelial changes in a murine model of atopic asthma [J].
Blyth, DI ;
Pedrick, MS ;
Savage, TJ ;
Hessel, EM ;
Fattah, D .
AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY, 1996, 14 (05) :425-438
[4]
Inflammatory stimuli induce accumulation of MHC class II complexes on dendritic cells [J].
Cella, M ;
Engering, A ;
Pinet, V ;
Pieters, J ;
Lanzavecchia, A .
NATURE, 1997, 388 (6644) :782-787
[5]
Cerwenka A, 1998, J IMMUNOL, V161, P97
[6]
BRONCHIAL REACTIVITY TO INHALED HISTAMINE - METHOD AND CLINICAL SURVEY [J].
COCKCROFT, DW ;
KILLIAN, DN ;
MELLON, JJA ;
HARGREAVE, FE .
CLINICAL ALLERGY, 1977, 7 (03) :235-243
[7]
VIRUS-SPECIFIC CD8(+) CELLS CAN SWITCH TO INTERLEUKIN-5 PRODUCTION AND INDUCE AIRWAY EOSINOPHILIA [J].
COYLE, AJ ;
ERARD, F ;
BERTRAND, C ;
WALTI, S ;
PIRCHER, H ;
LEGROS, G .
JOURNAL OF EXPERIMENTAL MEDICINE, 1995, 181 (03) :1229-1233
[8]
SYNAPSIN-I (PROTEIN-I), A NERVE TERMINAL-SPECIFIC PHOSPHOPROTEIN .1. ITS GENERAL DISTRIBUTION IN SYNAPSES OF THE CENTRAL AND PERIPHERAL NERVOUS-SYSTEM DEMONSTRATED BY IMMUNOFLUORESCENCE IN FROZEN AND PLASTIC SECTIONS [J].
DECAMILLI, P ;
CAMERON, R ;
GREENGARD, P .
JOURNAL OF CELL BIOLOGY, 1983, 96 (05) :1337-1354
[9]
DEVELOPMENT OF ALLERGY IN CHILDREN .1. ASSOCIATION WITH VIRUS-INFECTIONS [J].
FRICK, OL ;
GERMAN, DF ;
MILLS, J .
JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY, 1979, 63 (04) :228-241
[10]
ALLERGEN-INDUCED RECRUITMENT OF BRONCHOALVEOLAR HELPER (OKT4) AND SUPPRESSOR (OKT8) T-CELLS IN ASTHMA - RELATIVE INCREASES IN OKT8 CELLS IN SINGLE EARLY RESPONDERS COMPARED WITH THOSE IN LATE-PHASE RESPONDERS [J].
GONZALEZ, MC ;
DIAZ, P ;
GALLEGUILLOS, FR ;
ANCIC, P ;
CROMWELL, O ;
KAY, AB .
AMERICAN REVIEW OF RESPIRATORY DISEASE, 1987, 136 (03) :600-604