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

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Please use this identifier to cite or link to this item:http://hdl.handle.net/2115/86347

Title: Compartmentalization of interleukin 36 subfamily according to inducible and constitutive expression in the kidneys of a murine autoimmune nephritis model
Authors: Namba, Takashi Browse this author
Ichii, Osamu Browse this author →KAKEN DB
Nakamura, Teppei Browse this author →KAKEN DB
Masum, Md Abdul Browse this author
Otani, Yuki Browse this author
Hosotani, Marina Browse this author
Elewa, Yaser Hosny Ali Browse this author →ORCID
Kon, Yasuhiro Browse this author →KAKEN DB
Keywords: Nephritis
Systemic autoimmune disease
Chronic kidney disease
Inflammatory cytokine
Interleukin 36
Issue Date: 21-Jul-2021
Publisher: Springer
Journal Title: Cell and tissue research
Start Page: s00441-021-03495-8
Publisher DOI: 10.1007/s00441-021-03495-8
Abstract: 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.
Rights: 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
Type: article (author version)
URI: http://hdl.handle.net/2115/86347
Appears in Collections:獣医学院・獣医学研究院 (Graduate School of Veterinary Medicine / Faculty of Veterinary Medicine) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)

Submitter: 市居 修

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