CD100 boosts the inflammatory response in the challenge phase of allergic contact dermatitis in mice

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

Standard

CD100 boosts the inflammatory response in the challenge phase of allergic contact dermatitis in mice. / Mraz, Veronika; Funch, Anders B.; Jee, Mia H.; Gadsbøll, Anne Sofie Ø.; Weber, Julie F.; Yeung, Kelvin; Lohmann, Rebecca K.D.; Hawkes, Alana; Ødum, Niels; Woetmann, Anders; McKay, Dianne; Witherden, Deborah; Geisler, Carsten; Bonefeld, Charlotte M.

In: Contact Dermatitis, Vol. 89, No. 6, 2023, p. 442-452.

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

Harvard

Mraz, V, Funch, AB, Jee, MH, Gadsbøll, ASØ, Weber, JF, Yeung, K, Lohmann, RKD, Hawkes, A, Ødum, N, Woetmann, A, McKay, D, Witherden, D, Geisler, C & Bonefeld, CM 2023, 'CD100 boosts the inflammatory response in the challenge phase of allergic contact dermatitis in mice', Contact Dermatitis, vol. 89, no. 6, pp. 442-452. https://doi.org/10.1111/cod.14414

APA

Mraz, V., Funch, A. B., Jee, M. H., Gadsbøll, A. S. Ø., Weber, J. F., Yeung, K., Lohmann, R. K. D., Hawkes, A., Ødum, N., Woetmann, A., McKay, D., Witherden, D., Geisler, C., & Bonefeld, C. M. (2023). CD100 boosts the inflammatory response in the challenge phase of allergic contact dermatitis in mice. Contact Dermatitis, 89(6), 442-452. https://doi.org/10.1111/cod.14414

Vancouver

Mraz V, Funch AB, Jee MH, Gadsbøll ASØ, Weber JF, Yeung K et al. CD100 boosts the inflammatory response in the challenge phase of allergic contact dermatitis in mice. Contact Dermatitis. 2023;89(6):442-452. https://doi.org/10.1111/cod.14414

Author

Mraz, Veronika ; Funch, Anders B. ; Jee, Mia H. ; Gadsbøll, Anne Sofie Ø. ; Weber, Julie F. ; Yeung, Kelvin ; Lohmann, Rebecca K.D. ; Hawkes, Alana ; Ødum, Niels ; Woetmann, Anders ; McKay, Dianne ; Witherden, Deborah ; Geisler, Carsten ; Bonefeld, Charlotte M. / CD100 boosts the inflammatory response in the challenge phase of allergic contact dermatitis in mice. In: Contact Dermatitis. 2023 ; Vol. 89, No. 6. pp. 442-452.

Bibtex

@article{4c5aa2bb473f4a86a50a2e216a8817f0,
title = "CD100 boosts the inflammatory response in the challenge phase of allergic contact dermatitis in mice",
abstract = "Background: Allergic contact dermatitis (ACD) is an inflammatory disease with a complex pathophysiology in which epidermal-resident memory CD8+ T (TRM) cells play a key role. The mechanisms involved in the activation of CD8+ TRM cells during allergic flare-up responses are not understood. Methods: The expression of CD100 and its ligand Plexin B2 on CD8+ TRM cells and keratinocytes before and after allergen exposure was determined by flow cytometry and RT-qPCR. The role of CD100 in the inflammatory response during the challenge phase of ACD was determined in a model of ACD in CD100 knockout and wild-type mice. Results: We show that CD8+ TRM cells express CD100 during homeostatic conditions and up-regulate it following re-exposure of allergen-experienced skin to the experimental contact allergen 1-fluoro-2,4-dinitrobenzene (DNFB). Furthermore, Plexin B2 is up-regulated on keratinocytes following exposure to some contact allergens. We show that loss of CD100 results in a reduced inflammatory response to DNFB with impaired production of IFNγ, IL-17A, CXCL1, CXCL2, CXCL5, and IL-1β and decreased recruitment of neutrophils to the epidermis. Conclusion: Our study demonstrates that CD100 is expressed on CD8+ TRM cells and is required for full activation of CD8+ TRM cells and the flare-up response of ACD.",
keywords = "allergic contact dermatitis, CD100, CD8 T cells, plexin B2",
author = "Veronika Mraz and Funch, {Anders B.} and Jee, {Mia H.} and Gadsb{\o}ll, {Anne Sofie {\O}.} and Weber, {Julie F.} and Kelvin Yeung and Lohmann, {Rebecca K.D.} and Alana Hawkes and Niels {\O}dum and Anders Woetmann and Dianne McKay and Deborah Witherden and Carsten Geisler and Bonefeld, {Charlotte M.}",
note = "Publisher Copyright: {\textcopyright} 2023 The Authors. Contact Dermatitis published by John Wiley & Sons Ltd.",
year = "2023",
doi = "10.1111/cod.14414",
language = "English",
volume = "89",
pages = "442--452",
journal = "Contact Dermatitis. Supplement",
issn = "1396-6669",
publisher = "Wiley-Blackwell",
number = "6",

}

RIS

TY - JOUR

T1 - CD100 boosts the inflammatory response in the challenge phase of allergic contact dermatitis in mice

AU - Mraz, Veronika

AU - Funch, Anders B.

AU - Jee, Mia H.

AU - Gadsbøll, Anne Sofie Ø.

AU - Weber, Julie F.

AU - Yeung, Kelvin

AU - Lohmann, Rebecca K.D.

AU - Hawkes, Alana

AU - Ødum, Niels

AU - Woetmann, Anders

AU - McKay, Dianne

AU - Witherden, Deborah

AU - Geisler, Carsten

AU - Bonefeld, Charlotte M.

N1 - Publisher Copyright: © 2023 The Authors. Contact Dermatitis published by John Wiley & Sons Ltd.

PY - 2023

Y1 - 2023

N2 - Background: Allergic contact dermatitis (ACD) is an inflammatory disease with a complex pathophysiology in which epidermal-resident memory CD8+ T (TRM) cells play a key role. The mechanisms involved in the activation of CD8+ TRM cells during allergic flare-up responses are not understood. Methods: The expression of CD100 and its ligand Plexin B2 on CD8+ TRM cells and keratinocytes before and after allergen exposure was determined by flow cytometry and RT-qPCR. The role of CD100 in the inflammatory response during the challenge phase of ACD was determined in a model of ACD in CD100 knockout and wild-type mice. Results: We show that CD8+ TRM cells express CD100 during homeostatic conditions and up-regulate it following re-exposure of allergen-experienced skin to the experimental contact allergen 1-fluoro-2,4-dinitrobenzene (DNFB). Furthermore, Plexin B2 is up-regulated on keratinocytes following exposure to some contact allergens. We show that loss of CD100 results in a reduced inflammatory response to DNFB with impaired production of IFNγ, IL-17A, CXCL1, CXCL2, CXCL5, and IL-1β and decreased recruitment of neutrophils to the epidermis. Conclusion: Our study demonstrates that CD100 is expressed on CD8+ TRM cells and is required for full activation of CD8+ TRM cells and the flare-up response of ACD.

AB - Background: Allergic contact dermatitis (ACD) is an inflammatory disease with a complex pathophysiology in which epidermal-resident memory CD8+ T (TRM) cells play a key role. The mechanisms involved in the activation of CD8+ TRM cells during allergic flare-up responses are not understood. Methods: The expression of CD100 and its ligand Plexin B2 on CD8+ TRM cells and keratinocytes before and after allergen exposure was determined by flow cytometry and RT-qPCR. The role of CD100 in the inflammatory response during the challenge phase of ACD was determined in a model of ACD in CD100 knockout and wild-type mice. Results: We show that CD8+ TRM cells express CD100 during homeostatic conditions and up-regulate it following re-exposure of allergen-experienced skin to the experimental contact allergen 1-fluoro-2,4-dinitrobenzene (DNFB). Furthermore, Plexin B2 is up-regulated on keratinocytes following exposure to some contact allergens. We show that loss of CD100 results in a reduced inflammatory response to DNFB with impaired production of IFNγ, IL-17A, CXCL1, CXCL2, CXCL5, and IL-1β and decreased recruitment of neutrophils to the epidermis. Conclusion: Our study demonstrates that CD100 is expressed on CD8+ TRM cells and is required for full activation of CD8+ TRM cells and the flare-up response of ACD.

KW - allergic contact dermatitis

KW - CD100

KW - CD8 T cells

KW - plexin B2

U2 - 10.1111/cod.14414

DO - 10.1111/cod.14414

M3 - Journal article

C2 - 37700557

AN - SCOPUS:85170692942

VL - 89

SP - 442

EP - 452

JO - Contact Dermatitis. Supplement

JF - Contact Dermatitis. Supplement

SN - 1396-6669

IS - 6

ER -

ID: 371019449