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Blood, 1 February 2008, Vol. 111, No. 3, pp. 1489-1496.
Prepublished online as a Blood First Edition Paper on November 21, 2007; DOI 10.1182/blood-2007-07-102111.
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Submitted July 19, 2007
Accepted November 13, 2007
Indirect involvement of allergen-captured mast cells in antigen presentation
Taku Kambayashi, Jan D Baranski, Rebecca G Baker, Tao Zou, Eric J Allenspach, Jonathan E Shoag, Peter L Jones, and Gary A Koretzky*
Abramson Family Cancer Research Institute, University of Pennsylvania School of Medicine, Philadelphia, PA, United States
Department of Bioengineering, University of Pennsylvania, Philadelphia, PA, United States
Department of Medicine, University of Pennsylvania School of Medicine, Philadelphia, PA, United States
Institute for Medicine and Engineering, University of Pennsylvania, Philadelphia, PA, United States
Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, Philadelphia, PA, United States
* Corresponding author; email: koretzky{at}mail.med.upenn.edu.
It is generally believed that mast cells influence T cell activation non-specifically through the release of inflammatory mediators. In this report, we provide evidence that mast cells may also affect antigen-specific T cell responses by internalizing IgE-bound antigens for presentation to antigen-specific T cells. Surprisingly, T cell activation did not require that mast cells express MHC class II, indicating that mast cells were not involved in the direct presentation of the internalized antigens. Rather, the antigen captured by mast cells is presented by other MHC class II+ antigen-presenting cells. To explore how this may occur, we investigated the fate of mast cells stimulated by antigen and found that Fc RI crosslinking enhances mast cell apoptosis. Cell death by antigen-captured mast cells was required for efficient presentation, since protection of mast cell death significantly decreased T cell activation. These results suggest that mast cells may be involved in antigen presentation by acting as an antigen reservoir after antigen capture through specific IgE molecules bound to their Fc RI. This mechanism may contribute to the positive effect of mast cells on the development of T cell responses.

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