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Evidence for Interleukin-17C governing interleukin-17A pathogenicity and promoting asthma endotype switching in bronchiectasis
by
Lu, Hai-Wen
, Jiang, Fang
, Mao, Bei
, Wen, Yu-Hua
, Weng, Dong
, Gu, Shu-Yi
, Zhang, Yu-Wei
, Ge, Ai
, Ma, Jing-Ge
, Xie, Ying-Zhou
, Shen, Xi-Yue
, Sun, Xiao-Li
, Su, Yue
, Yang, Ling
, Qian, You-Cun
, Xu, Jin-Fu
in
13/1
/ 13/21
/ 13/31
/ 13/51
/ 38/77
/ 631/250/2504/2506
/ 631/250/347
/ 631/80/304
/ 64/60
/ 692/420/256/2515
/ 692/699/1785/31
/ 82/1
/ 82/29
/ 82/51
/ 96/109
/ Ablation
/ Adult
/ Aged
/ Animal models
/ Animals
/ Asthma
/ Asthma - complications
/ Asthma - immunology
/ Bronchiectasis
/ Bronchiectasis - complications
/ Bronchiectasis - immunology
/ Chronic infection
/ Cytokines
/ Disease Models, Animal
/ Female
/ Humanities and Social Sciences
/ Humans
/ Immunity, Innate
/ Infections
/ Interleukin-17 - genetics
/ Interleukin-17 - immunology
/ Interleukin-17 - metabolism
/ Interleukins
/ Lavage
/ Leukocytes (neutrophilic)
/ Lymphocytes - immunology
/ Lymphocytes - metabolism
/ Lymphoid cells
/ Male
/ Mice
/ Mice, Inbred C57BL
/ Middle Aged
/ multidisciplinary
/ Neutrophils
/ Ovalbumin
/ Pathogenicity
/ Pathogens
/ Peripheral blood
/ Pseudomonas aeruginosa
/ Pseudomonas aeruginosa - immunology
/ Pseudomonas Infections - immunology
/ Receptors, Interleukin-17 - genetics
/ Receptors, Interleukin-17 - metabolism
/ Respiratory tract
/ Respiratory tract infection
/ Science
/ Science (multidisciplinary)
/ Steroids
/ Therapeutic targets
2025
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Evidence for Interleukin-17C governing interleukin-17A pathogenicity and promoting asthma endotype switching in bronchiectasis
by
Lu, Hai-Wen
, Jiang, Fang
, Mao, Bei
, Wen, Yu-Hua
, Weng, Dong
, Gu, Shu-Yi
, Zhang, Yu-Wei
, Ge, Ai
, Ma, Jing-Ge
, Xie, Ying-Zhou
, Shen, Xi-Yue
, Sun, Xiao-Li
, Su, Yue
, Yang, Ling
, Qian, You-Cun
, Xu, Jin-Fu
in
13/1
/ 13/21
/ 13/31
/ 13/51
/ 38/77
/ 631/250/2504/2506
/ 631/250/347
/ 631/80/304
/ 64/60
/ 692/420/256/2515
/ 692/699/1785/31
/ 82/1
/ 82/29
/ 82/51
/ 96/109
/ Ablation
/ Adult
/ Aged
/ Animal models
/ Animals
/ Asthma
/ Asthma - complications
/ Asthma - immunology
/ Bronchiectasis
/ Bronchiectasis - complications
/ Bronchiectasis - immunology
/ Chronic infection
/ Cytokines
/ Disease Models, Animal
/ Female
/ Humanities and Social Sciences
/ Humans
/ Immunity, Innate
/ Infections
/ Interleukin-17 - genetics
/ Interleukin-17 - immunology
/ Interleukin-17 - metabolism
/ Interleukins
/ Lavage
/ Leukocytes (neutrophilic)
/ Lymphocytes - immunology
/ Lymphocytes - metabolism
/ Lymphoid cells
/ Male
/ Mice
/ Mice, Inbred C57BL
/ Middle Aged
/ multidisciplinary
/ Neutrophils
/ Ovalbumin
/ Pathogenicity
/ Pathogens
/ Peripheral blood
/ Pseudomonas aeruginosa
/ Pseudomonas aeruginosa - immunology
/ Pseudomonas Infections - immunology
/ Receptors, Interleukin-17 - genetics
/ Receptors, Interleukin-17 - metabolism
/ Respiratory tract
/ Respiratory tract infection
/ Science
/ Science (multidisciplinary)
/ Steroids
/ Therapeutic targets
2025
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Evidence for Interleukin-17C governing interleukin-17A pathogenicity and promoting asthma endotype switching in bronchiectasis
by
Lu, Hai-Wen
, Jiang, Fang
, Mao, Bei
, Wen, Yu-Hua
, Weng, Dong
, Gu, Shu-Yi
, Zhang, Yu-Wei
, Ge, Ai
, Ma, Jing-Ge
, Xie, Ying-Zhou
, Shen, Xi-Yue
, Sun, Xiao-Li
, Su, Yue
, Yang, Ling
, Qian, You-Cun
, Xu, Jin-Fu
in
13/1
/ 13/21
/ 13/31
/ 13/51
/ 38/77
/ 631/250/2504/2506
/ 631/250/347
/ 631/80/304
/ 64/60
/ 692/420/256/2515
/ 692/699/1785/31
/ 82/1
/ 82/29
/ 82/51
/ 96/109
/ Ablation
/ Adult
/ Aged
/ Animal models
/ Animals
/ Asthma
/ Asthma - complications
/ Asthma - immunology
/ Bronchiectasis
/ Bronchiectasis - complications
/ Bronchiectasis - immunology
/ Chronic infection
/ Cytokines
/ Disease Models, Animal
/ Female
/ Humanities and Social Sciences
/ Humans
/ Immunity, Innate
/ Infections
/ Interleukin-17 - genetics
/ Interleukin-17 - immunology
/ Interleukin-17 - metabolism
/ Interleukins
/ Lavage
/ Leukocytes (neutrophilic)
/ Lymphocytes - immunology
/ Lymphocytes - metabolism
/ Lymphoid cells
/ Male
/ Mice
/ Mice, Inbred C57BL
/ Middle Aged
/ multidisciplinary
/ Neutrophils
/ Ovalbumin
/ Pathogenicity
/ Pathogens
/ Peripheral blood
/ Pseudomonas aeruginosa
/ Pseudomonas aeruginosa - immunology
/ Pseudomonas Infections - immunology
/ Receptors, Interleukin-17 - genetics
/ Receptors, Interleukin-17 - metabolism
/ Respiratory tract
/ Respiratory tract infection
/ Science
/ Science (multidisciplinary)
/ Steroids
/ Therapeutic targets
2025
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Evidence for Interleukin-17C governing interleukin-17A pathogenicity and promoting asthma endotype switching in bronchiectasis
Journal Article
Evidence for Interleukin-17C governing interleukin-17A pathogenicity and promoting asthma endotype switching in bronchiectasis
2025
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Overview
The management of bronchiectasis-asthma overlap (BAO) is an important clinical issue to be addressed. Little is known regarding the endotype of BAO. Here we recruit patients with a primary diagnosis of bronchiectasis and co-existing asthma. The levels of interleukin (IL)-17C are positively correlated with the levels of IL-17A or group 3 innate lymphoid cells (ILC3s) in peripheral blood samples from patients with BAO. An in vivo mouse model of
Pseudomonas aeruginosa
chronic lower respiratory tract infection followed by ovalbumin-induced asthma shows that IL-17C potentiates IL-17A expression via interacting with IL-17 receptor E in ILC3s. Additionally, ablation of
Il17re
in mice attenuates ILC3 responses and IL-17A-mediated asthma endotype switching towards neutrophilic asthma driven by
P. aeruginosa
chronic lower respiratory tract infection. Lastly, impaired epithelial barrier integrity by
P. aeruginosa
exposure is associated with IL-17C production in vitro. Collectively, our study implicates evidence for IL-17C governing IL-17A pathogenicity and promoting asthma endotype switching in bronchiectasis, implicating IL-17C as a potential therapeutic target for individuals with BAO.
Bronchiectasis and asthma can co-exist in the same patient, and the characteristics may be different from bronchiectasis alone. Here the authors characterise the function of ILC3 cells and how IL-17C potentiates IL-17A expression promoting a neutrophil dominated asthma endotype in mouse bronchiectasis-asthma models.
Publisher
Nature Publishing Group UK,Nature Publishing Group,Nature Portfolio
Subject
/ 13/21
/ 13/31
/ 13/51
/ 38/77
/ 64/60
/ 82/1
/ 82/29
/ 82/51
/ 96/109
/ Ablation
/ Adult
/ Aged
/ Animals
/ Asthma
/ Bronchiectasis - complications
/ Female
/ Humanities and Social Sciences
/ Humans
/ Lavage
/ Male
/ Mice
/ Pseudomonas aeruginosa - immunology
/ Pseudomonas Infections - immunology
/ Receptors, Interleukin-17 - genetics
/ Receptors, Interleukin-17 - metabolism
/ Science
/ Steroids
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