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Title: Blocking B7 and CD40 co-stimulatory molecules decreases antiviral T cell activity
Authors: Vermeiren, Jan ×
Ceuppens, Jan
Haegel-Kronenberger, H
De Boer, M
Boon, L
Van Gool, Stefaan #
Issue Date: 21-Jan-2004
Series Title: Clinical and Experimental Immunology vol:135 issue:2 pages:253-8
Abstract: Inhibition of co-stimulatory signals for T cells by interrupting CD80/CD86-CD28 and CD40-CD154 interactions is a promising approach to prevent transplant rejection and to induce graft tolerance. However, this tolerizing treatment might affect T cell reactivity towards all the antigens to which the immune system is exposed during treatment. We addressed the question whether such inhibition of co-stimulatory ligands on human antigen presenting cells (APC) would affect T cell reactivity against a virus. This was tested in an in vitro system with freshly isolated human monocytes transduced with adenovirus (ad) containing either murine interferon-gamma (mIFN-gamma) or green fluorescent protein (GFP) as marker transgene. T cells co-cultured with transduced monocytes proliferated and produced cytokines. These 'primed' T cells had strong antiviral activity as they subsequently killed ad/GFP-transduced monocytes and reduced mIFN-gamma accumulation in coculture with ad/mIFN-transduced monocytes. However, if priming had occurred in the presence of blocking anti-CD40/CD80/CD86 MoAbs, generation of this antiviral activity was completely prevented. Moreover, T cells primed in the absence of co-stimulatory cells failed to proliferate upon restimulation with adenovirus-transduced monocytes. The results confirm that co-stimulatory signals from APC are required for efficient induction of antiviral T cell activity and point to a potential infectious risk of blocking co-stimulatory signals.
ISSN: 0009-9104
Publication status: published
KU Leuven publication type: IT
Appears in Collections:Pediatric Hematology & Oncology Section (-)
Laboratory of Clinical Immunology
Section Child - Miscellaneous (-)
Laboratory of Pediatric Immunology
× corresponding author
# (joint) last author

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