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CD4+ T cells play an essential role in chronic MC903-induced skin inflammation
Song, Mi Hye Gupta, Anupriya Sasidharan Nair, Varun Oh, Kwonik
Song, Mi Hye
Gupta, Anupriya
Sasidharan Nair, Varun
Oh, Kwonik
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Issue Date
2022-04-25
Submitted date
2022-04-05
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Abstract
MC903 skin inflammation model is one of well-characterized murine models of atopic dermatitis and driven by TSLP-mediated type 2 inflammation. Since it can be prepared simply by repetitive applications of MC903 and shows consistent clinical results, this model has been widely used. However, in contrast to human atopic dermatitis which is chronic and closely related to TH2 cells, MC903 induces inflammations temporarily and even in the absence of T cells. Here, we modified the MC903 treatment schedule and developed a chronic MC903-induced skin inflammation model. Mice were sensitized with a high dose of MC903 and challenged with a low dose of MC903. Prior to challenge, mice were allowed to recover completely from the inflammation which occurred during the sensitization. The challenge of MC903 induced skin swelling and type 2 inflammations more rapidly, which was dependent on CD4+ T cells and IL-33. We expect that our mouse model will be beneficial for studying the late course of atopic dermatitis. Keywords: Atopic dermatitis; CD4(+) T cell; Challenge; IL-33; MC903; Sensitization. Copyright © 2022 Elsevier Inc. All rights reserved.
Citation
Song MH, Gupta A, Sasidharan Nair V, Oh K. CD4+ T cells play an essential role in chronic MC903-induced skin inflammation. Biochem Biophys Res Commun. 2022 Jul 5;612:8-14. doi: 10.1016/j.bbrc.2022.04.106. Epub 2022 Apr 25. PMID: 35500442.
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MC903 skin inflammation model is one of well-characterized murine models of atopic dermatitis and driven by TSLP-mediated type 2 inflammation. Since it can be prepared simply by repetitive applications of MC903 and shows consistent clinical results, this model has been widely used. However, in contrast to human atopic dermatitis which is chronic and closely related to TH2 cells, MC903 induces inflammations temporarily and even in the absence of T cells. Here, we modified the MC903 treatment schedule and developed a chronic MC903-induced skin inflammation model. Mice were sensitized with a high dose of MC903 and challenged with a low dose of MC903. Prior to challenge, mice were allowed to recover completely from the inflammation which occurred during the sensitization. The challenge of MC903 induced skin swelling and type 2 inflammations more rapidly, which was dependent on CD4+ T cells and IL-33. We expect that our mouse model will be beneficial for studying the late course of atopic dermatitis.
Series/Report no.
Vol. 6
ISSN
0006291X
0006-291X
0006-291X
EISSN
10902104
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Gov't Doc #
Sponsors
National Research Foundation of Korea
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Attribution-NonCommercial 4.0 International