IL-17C is required for lethal inflammation during systemic fungal infection

Jinling Huang; Shaoshuai Meng; Shanjuan Hong; Xin Lin; Wei Jin; Chen Dong

doi:10.1038/cmi.2015.56

IL-17C is required for lethal inflammation during systemic fungal infection

Jinling Huang, Shaoshuai Meng, Shanjuan Hong, Xin Lin, Wei Jin, Chen Dong

Research output: Contribution to journal › Article › peer-review

47 Scopus citations

Abstract

Within the interleukin-17 (IL-17) family of cytokines, IL-17A is known to be critical in the host defense against fungal infections; however, the function of the other IL-17 family members in anti-fungal immunity remains largely unknown. Here, we show that IL-17C expression was highly induced in kidney epithelial cells after fungal infection. Mice that lacked IL-17C exhibited increased survival and attenuated kidney tissue damage, although they had similar fungal loads. IL-17C deficiency resulted in decreased pro-inflammatory cytokine expression compared with wild-type control mice. Additionally, IL-17C directly acted on renal epithelial cells in vitro to promote pro-inflammatory cytokine production. Taken together, our data demonstrate that IL-17C is a critical factor that potentiates inflammatory responses and causes host injury during fungal infection.

Original language	English (US)
Pages (from-to)	474-483
Number of pages	10
Journal	Cellular and Molecular Immunology
Volume	13
Issue number	4
DOIs	https://doi.org/10.1038/cmi.2015.56
State	Published - Jul 1 2016

Keywords

Fungal infection
IL-17C
kidney injury
pro-inflammatory cytokine
sepsis

ASJC Scopus subject areas

Immunology and Allergy
Immunology
Infectious Diseases

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10.1038/cmi.2015.56

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title = "IL-17C is required for lethal inflammation during systemic fungal infection",

abstract = "Within the interleukin-17 (IL-17) family of cytokines, IL-17A is known to be critical in the host defense against fungal infections; however, the function of the other IL-17 family members in anti-fungal immunity remains largely unknown. Here, we show that IL-17C expression was highly induced in kidney epithelial cells after fungal infection. Mice that lacked IL-17C exhibited increased survival and attenuated kidney tissue damage, although they had similar fungal loads. IL-17C deficiency resulted in decreased pro-inflammatory cytokine expression compared with wild-type control mice. Additionally, IL-17C directly acted on renal epithelial cells in vitro to promote pro-inflammatory cytokine production. Taken together, our data demonstrate that IL-17C is a critical factor that potentiates inflammatory responses and causes host injury during fungal infection.",

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AU - Huang, Jinling

AU - Meng, Shaoshuai

AU - Hong, Shanjuan

AU - Lin, Xin

AU - Jin, Wei

AU - Dong, Chen

PY - 2016/7/1

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N2 - Within the interleukin-17 (IL-17) family of cytokines, IL-17A is known to be critical in the host defense against fungal infections; however, the function of the other IL-17 family members in anti-fungal immunity remains largely unknown. Here, we show that IL-17C expression was highly induced in kidney epithelial cells after fungal infection. Mice that lacked IL-17C exhibited increased survival and attenuated kidney tissue damage, although they had similar fungal loads. IL-17C deficiency resulted in decreased pro-inflammatory cytokine expression compared with wild-type control mice. Additionally, IL-17C directly acted on renal epithelial cells in vitro to promote pro-inflammatory cytokine production. Taken together, our data demonstrate that IL-17C is a critical factor that potentiates inflammatory responses and causes host injury during fungal infection.

AB - Within the interleukin-17 (IL-17) family of cytokines, IL-17A is known to be critical in the host defense against fungal infections; however, the function of the other IL-17 family members in anti-fungal immunity remains largely unknown. Here, we show that IL-17C expression was highly induced in kidney epithelial cells after fungal infection. Mice that lacked IL-17C exhibited increased survival and attenuated kidney tissue damage, although they had similar fungal loads. IL-17C deficiency resulted in decreased pro-inflammatory cytokine expression compared with wild-type control mice. Additionally, IL-17C directly acted on renal epithelial cells in vitro to promote pro-inflammatory cytokine production. Taken together, our data demonstrate that IL-17C is a critical factor that potentiates inflammatory responses and causes host injury during fungal infection.

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IL-17C is required for lethal inflammation during systemic fungal infection

Abstract

Keywords

ASJC Scopus subject areas

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