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Title: Blockade of CTLA-4 enhances allergic sensitization and eosinophilic airway inflammation in genetically predisposed mice
Authors: Hellings, Peter ×
Vandenberghe, Peter
Kasran, Ahmad
Coorevits, Lieve
Overbergh, Lutgart
Mathieu, Chantal
Ceuppens, Jan #
Issue Date: Feb-2002
Series Title: European Journal of Immunology vol:32 issue:2 pages:585-94
Abstract: CTLA-4 (CD152) expression is restricted to subsets of activated T lymphocytes and shares homology with CD28. CTLA-4 and CD28 molecules both bind to B7 molecules on antigen-presenting cells. Whereas CD28-B7 interaction enhances T cell activation, cytokine production and survival, CTLA-4 signaling down-regulates T cell responses. Here, we studied the involvement of CTLA-4 triggering in the pathogenesis of allergen-induced airway inflammation in mice. Anti-CTLA-4 mAb were injected during i.p. sensitization with ovalbumin (OVA). This treatment favored OVA-specific IgE production and augmented blood eosinophilia in BALB/c mice. In BALB/c mice, enhanced Th2 sensitization after anti-CTLA-4 mAb injections resulted in more severe airway inflammation, and increased airway hyperresponsiveness to metacholine, bronchial eosinophilia and IL-4 and IL-5 levels in broncho-alveolar lavage (BAL) fluid following repeated allergen inhalations. Importantly, aggravation of airway inflammation and enhancement of Th2 responses were accompanied by a significant reduction of pulmonary TGF-beta levels at protein level in BAL fluid as well as on mRNA level in inflamed lung tissue. In contrast to BALB/c mice, blockade of CTLA-4 did not alter IgE production nor the phenotype of airway inflammation or TGF-beta production in C57BL/6 mice. Our data suggest that CTLA-4 triggering represents an important regulatory mechanism for Th2 sensitization in genetically predisposed mice by modulating TGF-beta production.
URI: 
ISSN: 0014-2980
Publication status: published
KU Leuven publication type: IT
Appears in Collections:Clinical Genetics Section (-)
Clinical and Experimental Endocrinology
Laboratory of Clinical Immunology
Research Group Experimental Oto-rhino-laryngology
Department of Human Genetics - miscellaneous
× corresponding author
# (joint) last author

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