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Blood, 1 August 2007, Vol. 110, No. 3, pp. 946-953.
Prepublished online as a Blood First Edition Paper on April 19, 2007; DOI 10.1182/blood-2006-07-036889.
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Submitted July 21, 2006
Accepted April 16, 2007
Mast cells are crucial for early inflammation, migration of Langerhans cells and CTL responses following topical application of TLR7 ligand in mice
Valeska Heib, Marc Becker, Tobias Warger, Gerd Rechtsteiner, Christine Tertilt, Matthias Klein, Tobias Bopp, Christian Taube, Hansjorg Schild, Edgar Schmitt, and Michael Stassen*
Institute for Immunology, Johannes Gutenberg University, Mainz, Germany
III. Medical Clinic, University of Mainz, Mainz, Germany
* Corresponding author; email: stassenm{at}uni-mainz.de.
Until recently, IgE-activated mast cells have been regarded merely as effector cells of adaptive immune responses, involved in allergic reactions and mucosal immunity to parasites. Herein we report that murine dermal mast cells, activated by local administration of a creme containing the synthetic TLR7 ligand imiquimod, are essential to initiate an early inflammatory reaction. The mast cell-derived cytokines TNF- and IL-1 play an important role in this process. Furthermore, TLR7 activated mast cells are also able to promote the emigration of Langerhans cells, which partly depends on the expression of mast cell-derived IL-1 We have previously shown that TLR7 ligation enhances transcutaneous immunization evoked by topical application of vaccine antigens to the skin, a procedure which directy targets skin-resident antigen presenting cells. Consequently, we now demonstrate here that the capacity to mount a peptide-specific cytotoxic T lymphocyte response following transcutaneous immunization employing imiquimod as adjuvant is severely impaired in mast cell-deficient mice. Thus, these findings demonstrate the potent versability of alternatively activated mast cells at the interface of innate and adaptive immunity.
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