T cell-independent mechanisms associated with neutrophil extracellular trap formation and selective autophagy in IL-17A-mediated epidermal hyperplasia

Erika Suzuki, Emanual Michael Maverakis, Ritu Sarin, Laura Bouchareychas, Vijay K. Kuchroo, Frank O. Nestle, Iannis Adamopoulos

Research output: Contribution to journalArticle

10 Citations (Scopus)

Abstract

IL-17A has been strongly associated with epidermal hyperplasia in many cutaneous disorders. However, because IL-17A is mainly produced by ab and ≥mma;δT cells in response to IL-23, the role of T cells and IL-23 has overshadowed any IL-17A-independent actions. In this article, we report that IL-17A gene transfer induces epidermal hyperplasia in Il23r-/-Rag1-/- and Tcrd-deficient mice, which can be prevented by neutrophil depletion. Moreover, adoptive transfer of CD11b+Gr-1hi cells, after IL-17A gene transfer, was sufficient to phenocopy the disease. We further show that the IL-17A-induced pathology was prevented in transgenic mice with impaired neutrophil extracellular trap formation and/or neutrophils with conditional deletion of the master regulator of selective autophagy, Wdfy3. Our data demonstrate a novel T cell-independent mechanism that is associated with neutrophil extracellular trap formation and selective autophagy in IL-17A-mediated epidermal hyperplasia.

Original languageEnglish (US)
Pages (from-to)4403-4412
Number of pages10
JournalJournal of Immunology
Volume197
Issue number11
DOIs
StatePublished - Dec 1 2016

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Interleukin-17
Autophagy
Hyperplasia
T-Lymphocytes
Interleukin-23
Neutrophils
Adoptive Transfer
Extracellular Traps
Transgenic Mice
Genes
Pathology
Skin

ASJC Scopus subject areas

  • Immunology

Cite this

T cell-independent mechanisms associated with neutrophil extracellular trap formation and selective autophagy in IL-17A-mediated epidermal hyperplasia. / Suzuki, Erika; Maverakis, Emanual Michael; Sarin, Ritu; Bouchareychas, Laura; Kuchroo, Vijay K.; Nestle, Frank O.; Adamopoulos, Iannis.

In: Journal of Immunology, Vol. 197, No. 11, 01.12.2016, p. 4403-4412.

Research output: Contribution to journalArticle

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abstract = "IL-17A has been strongly associated with epidermal hyperplasia in many cutaneous disorders. However, because IL-17A is mainly produced by ab and ≥mma;δT cells in response to IL-23, the role of T cells and IL-23 has overshadowed any IL-17A-independent actions. In this article, we report that IL-17A gene transfer induces epidermal hyperplasia in Il23r-/-Rag1-/- and Tcrd-deficient mice, which can be prevented by neutrophil depletion. Moreover, adoptive transfer of CD11b+Gr-1hi cells, after IL-17A gene transfer, was sufficient to phenocopy the disease. We further show that the IL-17A-induced pathology was prevented in transgenic mice with impaired neutrophil extracellular trap formation and/or neutrophils with conditional deletion of the master regulator of selective autophagy, Wdfy3. Our data demonstrate a novel T cell-independent mechanism that is associated with neutrophil extracellular trap formation and selective autophagy in IL-17A-mediated epidermal hyperplasia.",
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AU - Suzuki, Erika

AU - Maverakis, Emanual Michael

AU - Sarin, Ritu

AU - Bouchareychas, Laura

AU - Kuchroo, Vijay K.

AU - Nestle, Frank O.

AU - Adamopoulos, Iannis

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AB - IL-17A has been strongly associated with epidermal hyperplasia in many cutaneous disorders. However, because IL-17A is mainly produced by ab and ≥mma;δT cells in response to IL-23, the role of T cells and IL-23 has overshadowed any IL-17A-independent actions. In this article, we report that IL-17A gene transfer induces epidermal hyperplasia in Il23r-/-Rag1-/- and Tcrd-deficient mice, which can be prevented by neutrophil depletion. Moreover, adoptive transfer of CD11b+Gr-1hi cells, after IL-17A gene transfer, was sufficient to phenocopy the disease. We further show that the IL-17A-induced pathology was prevented in transgenic mice with impaired neutrophil extracellular trap formation and/or neutrophils with conditional deletion of the master regulator of selective autophagy, Wdfy3. Our data demonstrate a novel T cell-independent mechanism that is associated with neutrophil extracellular trap formation and selective autophagy in IL-17A-mediated epidermal hyperplasia.

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