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Transfer of allergic airway responses with antigen-primed CD4+ but not CD8+ T cells in brown Norway rats.
J Clin Invest. 1995 Sep;96(3):1303-10
Publication Type
A. Watanabe
H. Mishima
P M Renzi
L J Xu
Q. Hamid
J G Martin
Author Affiliation
Meakins-Christie Laboratories, Royal Victoria Hospital, McGill University, Montreal, Quebec, Canada.
J Clin Invest. 1995 Sep;96(3):1303-10
Publication Type
Allergens - immunology
Bronchoalveolar Lavage Fluid - cytology
CD4-Positive T-Lymphocytes - immunology
CD8-Positive T-Lymphocytes - immunology
Comparative Study
Eosinophils - cytology - immunology
Hypersensitivity - immunology
Immunity, Cellular
Immunoglobulin E - analysis
Immunotherapy, Adoptive
Leukocyte Count
Lung - immunology
Lymph Nodes - immunology
Lymphocyte Activation
Lymphocyte Transfusion
Ovalbumin - immunology
Rats, Inbred BN
Research Support, Non-U.S. Gov't
Respiratory System - immunology
Serum Albumin, Bovine - immunology
Skin Tests
T-Lymphocyte Subsets - immunology
Activated CD4+ helper T cells have been demonstrated in asthmatic airways and postulated to play a central role in eliciting allergic inflammation; direct evidence of their involvement seems to be lacking. We hypothesized that CD4+ T cells have the potential to induce allergic responses to antigen challenge, and tested this hypothesis in a model of allergic bronchoconstriction, the Brown Norway rat, using the approach of adoptive transfer. Animals were actively sensitized to either ovalbumin (OVA) or BSA and were used as donors of T cells. W3/25(CD4)+ or OX8(CD8)+ T cells were isolated from the cervical lymph nodes of sensitized donors and transferred to naive BN rats. 2 d after adoptive transfer recipient rats were challenged by OVA inhalation, and changes in lung resistance (RL), bronchoalveolar lavage (BAL) cells, and serum levels of antigen-specific IgE were studied. After OVA challenge recipients of OVA-primed W3/25+ T cells exhibited sustained increases in RL throughout the entire 8-h observation period and had significant bronchoalveolar lavage eosinophilia, which was detected by immunocytochemistry using an antimajor basic protein mAb. Recipients of BSA-primed W3/25+ T cells or OVA-primed OX8+ T cells failed to respond to inhaled OVA. OVA-specific immunoglobulin E was undetectable by ELISA or skin testing in any of the recipient rats after adoptive transfer. In conclusion, antigen-induced airway bronchoconstriction and eosinophilia were successfully transferred by antigen-specific W3/25+ T cells in Brown Norway rats. These responses were dependent on antigen-primed W3/25+ T cells and appeared to be independent of IgE-mediated mast cell activation. This study provides clear evidence for T cell mediated immune mechanisms in allergic airway responses in this experimental model.
PubMed ID
7657805 View in PubMed
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