NKG2D-Dependent Activation of Dendritic Epidermal T cells in Contact Hypersensitivity

Research output: Contribution to journal › Journal article › Research › peer-review

Standard

NKG2D-Dependent Activation of Dendritic Epidermal T cells in Contact Hypersensitivity. / Nielsen, Morten Milek; Dyring-Andersen, Beatrice; Schmidt, Jonas Damgård; Witherden, Deborah; Lovato, Paola; Woetmann, Anders ; Ødum, Niels; Poulsen, Steen Seier; Havran, Wendy L; Geisler, Carsten; Bonefeld, Charlotte Menné.

In: Journal of Investigative Dermatology, Vol. 135, No. 5, 05.2015, p. 1311-19.

Research output: Contribution to journal › Journal article › Research › peer-review

Harvard

Nielsen, MM, Dyring-Andersen, B, Schmidt, JD, Witherden, D, Lovato, P, Woetmann, A, Ødum, N, Poulsen, SS, Havran, WL, Geisler, C & Bonefeld, CM 2015, 'NKG2D-Dependent Activation of Dendritic Epidermal T cells in Contact Hypersensitivity', Journal of Investigative Dermatology, vol. 135, no. 5, pp. 1311-19. https://doi.org/10.1038/jid.2015.23

APA

Nielsen, M. M., Dyring-Andersen, B., Schmidt, J. D., Witherden, D., Lovato, P., Woetmann, A., Ødum, N., Poulsen, S. S., Havran, W. L., Geisler, C., & Bonefeld, C. M. (2015). NKG2D-Dependent Activation of Dendritic Epidermal T cells in Contact Hypersensitivity. Journal of Investigative Dermatology, 135(5), 1311-19. https://doi.org/10.1038/jid.2015.23

Vancouver

Nielsen MM, Dyring-Andersen B, Schmidt JD, Witherden D, Lovato P, Woetmann A et al. NKG2D-Dependent Activation of Dendritic Epidermal T cells in Contact Hypersensitivity. Journal of Investigative Dermatology. 2015 May;135(5):1311-19. https://doi.org/10.1038/jid.2015.23

Author

Nielsen, Morten Milek ; Dyring-Andersen, Beatrice ; Schmidt, Jonas Damgård ; Witherden, Deborah ; Lovato, Paola ; Woetmann, Anders ; Ødum, Niels ; Poulsen, Steen Seier ; Havran, Wendy L ; Geisler, Carsten ; Bonefeld, Charlotte Menné. / NKG2D-Dependent Activation of Dendritic Epidermal T cells in Contact Hypersensitivity. In: Journal of Investigative Dermatology. 2015 ; Vol. 135, No. 5. pp. 1311-19.

Bibtex

@article{08cf29fe01e647ae8cd1f0990314a43a,
title = "NKG2D-Dependent Activation of Dendritic Epidermal T cells in Contact Hypersensitivity",
abstract = "The interaction between keratinocytes (KC) and skin-resident immune cells plays an important role in induction of contact hypersensitivity (CHS). A specific subset of γδ T cells termed dendritic epidermal T cells (DETC) are located in mouse epidermis, and we have recently shown that DETC become activated and produce IL-17 in an IL-1β-dependent manner during CHS. Various receptors on DETC, including NKG2D, are involved in DETC responses against tumors and during wound healing. The ligands for NKG2D (NKG2DL) are stress-induced proteins such as Mult-1, H60, Rae-1 in mice and MICA, MICB and ULBP in humans. Here, we show that allergens up-regulate expression of the NKG2DL Mult-1, H60 and Rae-1 in cultured mouse KC and of MICA in primary human KC. We demonstrate that Mult-1 is expressed in mouse skin exposed to allergen. Furthermore, we find that the vast majority of DETC in murine epidermis and skin-homing cutaneous lymphocyte-associated antigen (CLA) positive γδ T cells in humans express NKG2D. Finally, we demonstrate that blocking of NKG2D partially inhibits allergen-induced DETC activation. These findings demonstrate that NKG2D and NKG2DL are involved in allergen-induced activation of DETC and indicate that the NKG2D/NKG2DL pathway might be a potential target for treatment of CHS.Journal of Investigative Dermatology accepted article preview online, 29 January 2015. doi:10.1038/jid.2015.23.",
author = "Nielsen, {Morten Milek} and Beatrice Dyring-Andersen and Schmidt, {Jonas Damg{\aa}rd} and Deborah Witherden and Paola Lovato and Anders Woetmann and Niels {\O}dum and Poulsen, {Steen Seier} and Havran, {Wendy L} and Carsten Geisler and Bonefeld, {Charlotte Menn{\'e}}",
year = "2015",
month = may,
doi = "10.1038/jid.2015.23",
language = "English",
volume = "135",
pages = "1311--19",
journal = "Journal of Investigative Dermatology",
issn = "0022-202X",
publisher = "nature publishing group",
number = "5",

}

RIS

TY - JOUR

T1 - NKG2D-Dependent Activation of Dendritic Epidermal T cells in Contact Hypersensitivity

AU - Nielsen, Morten Milek

AU - Dyring-Andersen, Beatrice

AU - Schmidt, Jonas Damgård

AU - Witherden, Deborah

AU - Lovato, Paola

AU - Woetmann, Anders

AU - Ødum, Niels

AU - Poulsen, Steen Seier

AU - Havran, Wendy L

AU - Geisler, Carsten

AU - Bonefeld, Charlotte Menné

PY - 2015/5

Y1 - 2015/5

N2 - The interaction between keratinocytes (KC) and skin-resident immune cells plays an important role in induction of contact hypersensitivity (CHS). A specific subset of γδ T cells termed dendritic epidermal T cells (DETC) are located in mouse epidermis, and we have recently shown that DETC become activated and produce IL-17 in an IL-1β-dependent manner during CHS. Various receptors on DETC, including NKG2D, are involved in DETC responses against tumors and during wound healing. The ligands for NKG2D (NKG2DL) are stress-induced proteins such as Mult-1, H60, Rae-1 in mice and MICA, MICB and ULBP in humans. Here, we show that allergens up-regulate expression of the NKG2DL Mult-1, H60 and Rae-1 in cultured mouse KC and of MICA in primary human KC. We demonstrate that Mult-1 is expressed in mouse skin exposed to allergen. Furthermore, we find that the vast majority of DETC in murine epidermis and skin-homing cutaneous lymphocyte-associated antigen (CLA) positive γδ T cells in humans express NKG2D. Finally, we demonstrate that blocking of NKG2D partially inhibits allergen-induced DETC activation. These findings demonstrate that NKG2D and NKG2DL are involved in allergen-induced activation of DETC and indicate that the NKG2D/NKG2DL pathway might be a potential target for treatment of CHS.Journal of Investigative Dermatology accepted article preview online, 29 January 2015. doi:10.1038/jid.2015.23.

AB - The interaction between keratinocytes (KC) and skin-resident immune cells plays an important role in induction of contact hypersensitivity (CHS). A specific subset of γδ T cells termed dendritic epidermal T cells (DETC) are located in mouse epidermis, and we have recently shown that DETC become activated and produce IL-17 in an IL-1β-dependent manner during CHS. Various receptors on DETC, including NKG2D, are involved in DETC responses against tumors and during wound healing. The ligands for NKG2D (NKG2DL) are stress-induced proteins such as Mult-1, H60, Rae-1 in mice and MICA, MICB and ULBP in humans. Here, we show that allergens up-regulate expression of the NKG2DL Mult-1, H60 and Rae-1 in cultured mouse KC and of MICA in primary human KC. We demonstrate that Mult-1 is expressed in mouse skin exposed to allergen. Furthermore, we find that the vast majority of DETC in murine epidermis and skin-homing cutaneous lymphocyte-associated antigen (CLA) positive γδ T cells in humans express NKG2D. Finally, we demonstrate that blocking of NKG2D partially inhibits allergen-induced DETC activation. These findings demonstrate that NKG2D and NKG2DL are involved in allergen-induced activation of DETC and indicate that the NKG2D/NKG2DL pathway might be a potential target for treatment of CHS.Journal of Investigative Dermatology accepted article preview online, 29 January 2015. doi:10.1038/jid.2015.23.

U2 - 10.1038/jid.2015.23

DO - 10.1038/jid.2015.23

M3 - Journal article

C2 - 25634359

VL - 135

SP - 1311

EP - 1319

JO - Journal of Investigative Dermatology

JF - Journal of Investigative Dermatology

SN - 0022-202X

IS - 5

ER -

ID: 130838332