Human keratinocytes release high levels of inducible heat shock protein 70 that enhances peptide uptake

Wang, Dong; Zeitvogel, Jana; Dressel, Ralf; Werfel, Thomas; Wittmann, Miriam

doi:10.1111/j.1600-0625.2011.01287.x

Cited by 12 publications

(8 citation statements)

References 48 publications

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“…Therefore, extracellular HSP70 has been recognized to act as a danger signal. In the context of skin inflammatory disorders, it was shown that keratinocytes are much more competent to release high levels of HSP70 compared with other cells such as fibroblasts, macrophages or PBMCs . Several environmental factors that affect the skin can trigger the release of HSP70 in the extracellular environment, such as heat, cold, chemicals, allergens and ultraviolet (UV) radiation .…”

Section: Discussionmentioning

confidence: 99%

Heat shock protein 70 potentiates interferon alpha production by plasmacytoid dendritic cells: relevance for cutaneous lupus and vitiligo pathogenesis

et al. 2017

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Section: Discussionmentioning

confidence: 99%

Heat shock protein 70 potentiates interferon alpha production by plasmacytoid dendritic cells: relevance for cutaneous lupus and vitiligo pathogenesis

et al. 2017

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“…In addition, this reduced skin barrier function is accompanied by thermal stress induction that is represented by HSP70. In infl ammatory skin diseases with reduced skin barrier function like psoriasis and atopic dermatitis HSP70 is also involved [ 14 ] . In contrast, water sprinkling of natural grass seems to prevent this sliding induced thermal stress induction and skin damage.…”

mentioning

confidence: 99%

The Potential of the Skin as a Readout System to Test Artificial Turf Systems: Clinical and Immunohistological Effects of a Sliding on Natural Grass and Artificial Turf

et al. 2013

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The purpose of this study was to investigate the interaction of skin with natural grass and artificial turf at clinical, histological and immunohistochemical level. Therefore, 14 male volunteers performed slidings on dry natural grass, wet natural grass and artificial turf. Directly and 24 h after the slidings, a clinical picture and a 3-mm punch biopsy of the lesion were taken. Paraffin sections (6 µm) were hematoxylin-eosin stained. Immunohistochemistry was performed for CD3, hBD-2, K16, K10, Ki67 and HSP70. Clinically, a sliding performed on artificial turf caused less erythema but more abrasion compared to natural grass. At histological level, artificial turf or dry natural grass damaged the stratum corneum the most. Directly after the sliding, CD3, hBD-2, K16, K10, Ki67 and HSP70 expression was normal. 24 h after a sliding on artificial turf or dry natural grass, an increase of K16, hBD-2 and HSP70 expression was observed. In this pilot study it was not possible to clearly distinguish between skin damage induced by a sliding on artificial turf and natural grass. However, small differences at clinical and histological level seem to exist. This demonstrates the potential of the skin as readout system to evaluate artificial turf systems and mechanical skin damage.

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“…Although HSP70 was found intracellularly, the secreted extracellular form of HSP70 was also recognized [43,44]. Secreted HSP70 is capable of binding to antigenic peptides and delivering them to DCs in a receptormediated manner [45,46]. Judging from both the cytoprotective and antioxidative roles of intracellular HSP70 and the immunostimulatory action by the extracellular form, HSP70 likely acts like a double-edged sword in the pathogenesis of CHS.…”

Section: Discussionmentioning

confidence: 99%

The Antioxidative Effect of Heat‐Shock Protein 70 in Dendritic Cells

Kim

Roh

et al. 2013

Scand J Immunol

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Reactive oxygen species (ROS) are produced by dendritic cells (DCs) during antigen presentation in contact hypersensitivity (CHS). ROS cause a number of non-enzymatic protein modifications, such as carbonylation. Carbonylated proteins in DCs in response to hapten have not been fully identified yet. To identify the proteins carbonylated by ROS, murine epidermis-derived DC line XS106 was challenged with a hapten, 2,4,6-trinitrobenzene sulphonic acid (TNBS). MALDI-TOF analysis revealed that heat-shock protein 70 (HSP70) was one of the carbonylated proteins induced by TNBS. To verify the role of HSP70 in TNBS-treated XS106 cell, we fused protein transduction domain (PTD) with HSP70 to facilitate protein delivery into the cell. The transfected fusion protein HSP70 within the cell caused transient increase of the cellular level of HSP70. Transient increase of HSP70 level in XS-106 DCs resulted in inhibition of ROS production, carbonylation of HSP70, p38 MAPK activation and subsequently IL-12 secretion. To investigate the effects of PTD-HSP70 in vivo, ear-swelling experiments with 2,4,6-trinitro-1-chlorobenzene (TNCB) were performed in BALB/c mice. Pretreatment of PTD-HSP70 reduced the CHS response to TNCB in vivo. We report here that carbonylation of HSP70 by ROS is associated with the pathogenesis of CHS, suggesting possibility of HSP70-targeting therapy in CHS.

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Human keratinocytes release high levels of inducible heat shock protein 70 that enhances peptide uptake

Abstract: Production and uptake of inducible HSP70 by keratinocytes may critically influence the chronic course of inflammatory skin diseases.

Cited by 12 publications

References 48 publications

Heat shock protein 70 potentiates interferon alpha production by plasmacytoid dendritic cells: relevance for cutaneous lupus and vitiligo pathogenesis

Heat shock protein 70 potentiates interferon alpha production by plasmacytoid dendritic cells: relevance for cutaneous lupus and vitiligo pathogenesis

The Potential of the Skin as a Readout System to Test Artificial Turf Systems: Clinical and Immunohistological Effects of a Sliding on Natural Grass and Artificial Turf

The Antioxidative Effect of Heat‐Shock Protein 70 in Dendritic Cells

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