ArticleThe Journal of investigative dermatology2013
TGFβ1 overexpression by keratinocytes alters skin dendritic cell homeostasis and enhances contact hypersensitivity.
Article in The Journal of investigative dermatology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
10 citing papers in PubMed, 23 citations in OpenAlex.
- A Comprehensive Assessment of the Biocompatibility and Safety of Diamond Nanoparticles on Reconstructed Human Epidermis.Materials (Basel, Switzerland) · 2023Article
- Peelable Microneedle Patches Deliver Fibroblast Growth Factors to Repair Skin Photoaging Damage.Nanotheranostics · 2023Article
- Phenotypical Conversions of Dermal Adipocytes as Pathophysiological Steps in Inflammatory Cutaneous Disorders.International journal of molecular sciences · 2022Review
- Skin Immunity and Tolerance: Focus on Epidermal Keratinocytes Expressing HLA-G.Frontiers in immunology · 2021Review
- Taking the lead - how keratinocytes orchestrate skin T cell immunity.Immunology letters · 2018Review
- Direct control of regulatory T cells by keratinocytes.Nature immunology · 2017Article
- Amelioration of patients with chronic spontaneous urticaria in treatment with vitamin D supplement.Clinical and molecular allergy : CMA · 2017Article
- Regulation of Dendritic Cell Function in Inflammation.Journal of immunology research · 2015Review
- Tumor-promoting role of TGFβ1 signaling in ultraviolet B-induced skin carcinogenesis is associated with cutaneous inflammation and lymph node migration of dermal dendritic cells.Carcinogenesis · 2014Article
- The Role of TGFβ Signaling in Squamous Cell Cancer: Lessons from Mouse Models.Journal of skin cancer · 2012Article
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6 authors at 2 institutions in 1 country.
Funding
Abstract
Overexpression of transforming growth factor beta-1 (TGFβ1) in mouse epidermis causes cutaneous inflammation and keratinocyte hyperproliferation. Here we examined acute effects of TGFβ1 overproduction by keratinocytes on skin dendritic cells (DCs). TGFβ1 induction for 2 and 4 days increased the numbers and CD86 expression of B220(+) plasmacytoid DCs (pDCs) and CD207(+)CD103(+), CD207(-)CD103(-)CD11b(+), and CD207(-)CD103(-)CD11b(-) dermal DCs (dDCs) in skin-draining lymph nodes (SDLNs). The dermis of TGFβ1-overexpressing mice had significantly more pDCs, CD207(+)CD103(+) dDCs, and CD207(-)CD11b(+) dDCs in the absence of increased dermal proliferation. Application of dye, tetramethyl rhodamine iso-thiocyanate (TRITC), in dibutylpthalate (DBP) solution after TGFβ1 induction increased the numbers of TRITC(+)CD207(-) dDCs in SDLNs, and augmented TRITC/DBP-induced Langerhans cell (LC) migration 72 hours post TRITC treatment. Consistent with this, LC migration was increased in vitro by TGFβ1 overexpression in skin explants and by exogenous TGFβ1 in culture media. Transient TGFβ1 induction during DNFB sensitization increased contact hypersensitivity responses by 1.5-fold. Thus, elevated epidermal TGFβ1 alone is sufficient to alter homeostasis of multiple cutaneous DC subsets, and enhance DC migration and immune responses to contact sensitizers. These results highlight a role for keratinocyte-derived TGFβ1 in DC trafficking and in the initiation of skin inflammation.
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Registered trials
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