IL-17RA is required for CCL2 expression, macrophage recruitment, and emphysema in response to cigarette smoke.
Chronic Obstructive Pulmonary Disease (COPD) is characterized by airspace enlargement and peribronchial lymphoid follicles; however, the immunological mechanisms leading to these pathologic changes remain undefined. Here we show that cigarette smoke is a selective adjuvant that augments in vitro and...
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Public Library of Science (PLoS)
2011
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oai:doaj.org-article:50301d1cf40c4f6384de173cb992c82e2021-11-18T06:52:58ZIL-17RA is required for CCL2 expression, macrophage recruitment, and emphysema in response to cigarette smoke.1932-620310.1371/journal.pone.0020333https://doaj.org/article/50301d1cf40c4f6384de173cb992c82e2011-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/21647421/?tool=EBIhttps://doaj.org/toc/1932-6203Chronic Obstructive Pulmonary Disease (COPD) is characterized by airspace enlargement and peribronchial lymphoid follicles; however, the immunological mechanisms leading to these pathologic changes remain undefined. Here we show that cigarette smoke is a selective adjuvant that augments in vitro and in vivo Th17, but not Th1, cell differentiation via the aryl hydrocarbon receptor. Smoke exposed IL-17RA(-/-) mice failed to induce CCL2 and MMP12 compared to WT mice. Remarkably, in contrast to WT mice, IL-17RA(-/-) mice failed to develop emphysema after 6 months of cigarette smoke exposure. Taken together, these data demonstrate that cigarette smoke is a potent Th17 adjuvant and that IL-17RA signaling is required for chemokine expression necessary for MMP12 induction and tissue emphysema.Kong ChenDerek A PociaskJeremy P McAleerYvonne R ChanJohn F AlcornJames L KreindlerMatthew R KeyserSteven D ShapiroA McGarry HoughtonJay K KollsMingquan ZhengPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 6, Iss 5, p e20333 (2011) |
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Medicine R Science Q Kong Chen Derek A Pociask Jeremy P McAleer Yvonne R Chan John F Alcorn James L Kreindler Matthew R Keyser Steven D Shapiro A McGarry Houghton Jay K Kolls Mingquan Zheng IL-17RA is required for CCL2 expression, macrophage recruitment, and emphysema in response to cigarette smoke. |
description |
Chronic Obstructive Pulmonary Disease (COPD) is characterized by airspace enlargement and peribronchial lymphoid follicles; however, the immunological mechanisms leading to these pathologic changes remain undefined. Here we show that cigarette smoke is a selective adjuvant that augments in vitro and in vivo Th17, but not Th1, cell differentiation via the aryl hydrocarbon receptor. Smoke exposed IL-17RA(-/-) mice failed to induce CCL2 and MMP12 compared to WT mice. Remarkably, in contrast to WT mice, IL-17RA(-/-) mice failed to develop emphysema after 6 months of cigarette smoke exposure. Taken together, these data demonstrate that cigarette smoke is a potent Th17 adjuvant and that IL-17RA signaling is required for chemokine expression necessary for MMP12 induction and tissue emphysema. |
format |
article |
author |
Kong Chen Derek A Pociask Jeremy P McAleer Yvonne R Chan John F Alcorn James L Kreindler Matthew R Keyser Steven D Shapiro A McGarry Houghton Jay K Kolls Mingquan Zheng |
author_facet |
Kong Chen Derek A Pociask Jeremy P McAleer Yvonne R Chan John F Alcorn James L Kreindler Matthew R Keyser Steven D Shapiro A McGarry Houghton Jay K Kolls Mingquan Zheng |
author_sort |
Kong Chen |
title |
IL-17RA is required for CCL2 expression, macrophage recruitment, and emphysema in response to cigarette smoke. |
title_short |
IL-17RA is required for CCL2 expression, macrophage recruitment, and emphysema in response to cigarette smoke. |
title_full |
IL-17RA is required for CCL2 expression, macrophage recruitment, and emphysema in response to cigarette smoke. |
title_fullStr |
IL-17RA is required for CCL2 expression, macrophage recruitment, and emphysema in response to cigarette smoke. |
title_full_unstemmed |
IL-17RA is required for CCL2 expression, macrophage recruitment, and emphysema in response to cigarette smoke. |
title_sort |
il-17ra is required for ccl2 expression, macrophage recruitment, and emphysema in response to cigarette smoke. |
publisher |
Public Library of Science (PLoS) |
publishDate |
2011 |
url |
https://doaj.org/article/50301d1cf40c4f6384de173cb992c82e |
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