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Fibroblasts support migration of monocyte‐derived dendritic cells by secretion of PGE 2 and MMP ‐1
Author(s) -
Saalbach Anja,
Janik Tobias,
Busch Matthias,
Herbert Diana,
Anderegg Ulf,
Simon Jan C.
Publication year - 2015
Publication title -
experimental dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.108
H-Index - 96
eISSN - 1600-0625
pISSN - 0906-6705
DOI - 10.1111/exd.12722
Subject(s) - dermal fibroblast , matrix metalloproteinase , fibroblast , microbiology and biotechnology , dendritic cell , immune system , inflammation , chemistry , secretion , immunology , dermis , stromal cell , collagenase , monocyte , biology , cancer research , biochemistry , in vitro , anatomy , enzyme
The outcome of a cutaneous immune response is critically dependent upon the ability of dendritic cells ( DC ) to migrate from skin to the draining lymph nodes – a process that is influenced by the cutaneous tissue microenvironment. Here, the role of fibroblasts – a major component of the dermal microenvironment – on the migratory capacity of monocyte‐derived DC (Mo DC ) was investigated in a 3D collagen I matrix. Indeed, dermal fibroblasts supported the migration of pre‐activated Mo DC through a 3D collagen I matrix. Activation of human Mo DC resulted in the release of TNF α and IL ‐1β that in turn stimulated MMP ‐1 (human collagenase) and PGE 2 secretion by human dermal fibroblasts. Transmigration assays confirmed the importance of fibroblast‐derived MMP ‐1 and PGE 2 for the migration of Mo DC through a 3D collagen I matrix. Finally, in mice initiation of inflammation by induction of an irritant contact dermatitis or a psoriasis‐like skin inflammation, the expression of the PGE 2 generating cox‐2 and the mouse collagen I degrading enzyme matrix metalloproteinases ( MMP )‐13 was strongly up‐regulated. Our study indicates that Mo DC are able to instruct dermal fibroblasts resulting in enhanced migratory capability of Mo DC , thus highlighting the role of a crosstalk of DC with their stromal microenvironment for the control of cutaneous immune responses.