Compartmentalization of interleukin 36 subfamily according to inducible and constitutive expression in the kidneys of a murine autoimmune nephritis model

Namba, Takashi; Ichii, Osamu; Nakamura, Teppei; Masum, Md Abdul; Otani, Yuki; Hosotani, Marina; Elewa, Yaser Hosny Ali; Kon, Yasuhiro

Compartmentalization of interleukin 36 subfamily according to inducible and constitutive expression in the kidneys of a murine autoimmune nephritis model

Namba, Takashi; Ichii, Osamu; Nakamura, Teppei et al.

Cell and tissue research, 2021, 386, 59-77

Permalink : https://hdl.handle.net/2115/86347

このアイテムのアクセス数:519件（2026-01-24 04:42 集計）

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アクセス権	open access
URI	https://hdl.handle.net/2115/86347
タイトル	Compartmentalization of interleukin 36 subfamily according to inducible and constitutive expression in the kidneys of a murine autoimmune nephritis model
著者	Namba, Takashi ; Ichii, Osamu ; Nakamura, Teppei ; Masum, Md Abdul ; Otani, Yuki ; Hosotani, Marina ; Elewa, Yaser Hosny Ali ; Kon, Yasuhiro
著者名 Namba, Takashi
e-Rad_Researcher 60547769 著者名 Ichii, Osamu
e-Rad_Researcher 80786773 著者名 Nakamura, Teppei
著者名 Masum, Md Abdul
著者名 Otani, Yuki
著者名 Hosotani, Marina
ORCID 0000-0002-7347-4587 著者名 Elewa, Yaser Hosny Ali
e-Rad_Researcher 10178402 著者名 Kon, Yasuhiro
言語	英語
キーワード	Nephritis
	Systemic autoimmune disease
	Chronic kidney disease
	Inflammatory cytokine
	Interleukin 36
発行日	2021-07-21
出版者	Springer
収録物名	Cell and tissue research
巻(号)	386
ページ	59-77
抄録	The interleukin (IL) 36 subfamily belongs to the IL-1 family and is comprised of agonists (IL-36 alpha, IL-36 beta, IL-36 gamma) and antagonists (IL-36Ra, IL-38). We previously reported IL-36 alpha overexpression in renal tubules of chronic nephritis mice. To understand the localization status and biological relationships among each member of the IL-36 subfamily in the kidneys, MRL/MpJ-Fas(lpr/lpr) mice were investigated as autoimmune nephritis models using pathology-based techniques. MRL/MpJ-Fas(lpr/lpr) mice exhibited disease onset from 3 months and severe nephritis at 6-7 months (early and late stages, respectively). Briefly, IL-36 gamma and IL-36Ra were constitutively expressed in murine kidneys, while the expression of IL-36 alpha, IL-36 beta, IL-36Ra, and IL-38 was induced in MRL/MpJ-Fas(lpr/lpr) mice. IL-36 alpha expression was significantly increased and localized to injured tubular epithelial cells (TECs). CD44(+)-activated parietal epithelial cells (PECs) also exhibited higher IL-36 alpha-positive rates, particularly in males. IL-36 beta and IL-38 are expressed in interstitial plasma cells. Quantitative indices for IL-36 alpha and IL-38 positively correlated with nephritis severity. Similar to IL-36 alpha, IL-36Ra localized to TECs and PECs at the late stage; however, MRL/MpJ-Fas(lpr/lpr) and healthy MRL/MpJ mice possessed IL-36Ra(+) smooth muscle cells in kidney arterial tunica media at both stages. IL-36 gamma was constitutively expressed in renal sympathetic axons regardless of strain and stage. IL-36 receptor gene was ubiquitously expressed in the kidneys and was induced proportional to disease severity. MRL/MpJ-Fas(lpr/lpr) mice kidneys possessed significantly upregulated IL-36 downstream candidates, including NF-kappa B- or MAPK-pathway organizing molecules. Thus, the IL-36 subfamily contributes to homeostasis and inflammation in the kidneys, and especially, an IL-36 alpha-dominant imbalance could strongly impact nephritis deterioration.
資源タイプ	学術雑誌論文
出版タイプ	Accepted Manuscript
権利情報	This is a post-peer-review, pre-copyedit version of an article published in Cell and tissue research. The final authenticated version is available online at: http://dx.doi.org/10.1007/s00441-021-03495-8
PISSN	0302-766X
関連情報 (isVersionOf)	出版社版DOI https://doi.org/10.1007/s00441-021-03495-8