IL-33–Mediated Expansion of Type 2 Innate Lymphoid Cells Protects from Progressive Glomerulosclerosis

先天性淋巴细胞 局灶节段性肾小球硬化 免疫系统 免疫学 白细胞介素33 髓样 先天免疫系统 炎症 生物 急性肾损伤 肾小球硬化 肾脏疾病 医学 肾小球肾炎 病理 白细胞介素 内科学 细胞因子 内分泌学 蛋白尿
作者
Jan-Hendrik Riedel,Martina Becker,Kerstin Kopp,Mathis Düster,Silke R. Brix,Catherine Meyer-Schwesinger,Luis Kluth,Ann-Christin Gnirck,Madena Attar,Sonja Krohn,Boris Fehse,Rolf A.K. Stahl,Ulf Panzer,Jan‐Eric Turner
出处
期刊:Journal of The American Society of Nephrology 卷期号:28 (7): 2068-2080 被引量:96
标识
DOI:10.1681/asn.2016080877
摘要

Innate lymphoid cells (ILCs) have an important role in the immune system's response to different forms of infectious and noninfectious pathologies. In particular, IL-5– and IL-13–producing type 2 ILCs (ILC2s) have been implicated in repair mechanisms that restore tissue integrity after injury. However, the presence of renal ILCs in humans has not been reported. In this study, we show that ILC populations are present in the healthy human kidney. A detailed characterization of kidney-residing ILC populations revealed that IL-33 receptor–positive ILC2s are a major ILC subtype in the kidney of humans and mice. Short-term IL-33 treatment in mice led to sustained expansion of IL-33 receptor–positive kidney ILC2s and ameliorated adriamycin-induced glomerulosclerosis. Furthermore, the expansion of ILC2s modulated the inflammatory response in the diseased kidney in favor of an anti-inflammatory milieu with a reduction of pathogenic myeloid cell infiltration and a marked accumulation of eosinophils that was required for tissue protection. In summary, kidney-residing ILC2s can be effectively expanded in the mouse kidney by IL-33 treatment and are central regulators of renal repair mechanisms. The presence of ILC2s in the human kidney tissue identifies these cells as attractive therapeutic targets for CKD in humans.
最长约 10秒,即可获得该文献文件

科研通智能强力驱动
Strongly Powered by AbleSci AI
科研通是完全免费的文献互助平台,具备全网最快的应助速度,最高的求助完成率。 对每一个文献求助,科研通都将尽心尽力,给求助人一个满意的交代。
实时播报
2秒前
3秒前
英姑应助LYJ采纳,获得10
3秒前
3秒前
liz发布了新的文献求助30
4秒前
冷静的若枫完成签到 ,获得积分10
5秒前
Leo完成签到,获得积分10
6秒前
biubiubiu完成签到,获得积分10
6秒前
zhenglinmama发布了新的文献求助10
7秒前
丢丢银发布了新的文献求助10
7秒前
陈文文完成签到 ,获得积分10
10秒前
10秒前
biubiubiu发布了新的文献求助10
11秒前
小二郎应助现代的天空采纳,获得10
15秒前
15秒前
20秒前
Micro_A应助科研通管家采纳,获得10
21秒前
李健应助科研通管家采纳,获得10
21秒前
大模型应助科研通管家采纳,获得10
21秒前
充电宝应助科研通管家采纳,获得10
21秒前
领导范儿应助科研通管家采纳,获得10
21秒前
FashionBoy应助科研通管家采纳,获得10
21秒前
Micro_A应助科研通管家采纳,获得10
21秒前
搜集达人应助科研通管家采纳,获得10
21秒前
传奇3应助科研通管家采纳,获得10
21秒前
科研通AI5应助科研通管家采纳,获得10
22秒前
隐形曼青应助科研通管家采纳,获得10
22秒前
华仔应助万幸鹿采纳,获得10
22秒前
搜集达人应助科研通管家采纳,获得10
22秒前
酷波er应助科研通管家采纳,获得10
22秒前
深情安青应助科研通管家采纳,获得10
22秒前
脑洞疼应助科研通管家采纳,获得10
22秒前
打打应助科研通管家采纳,获得10
22秒前
慕青应助科研通管家采纳,获得10
22秒前
烟花应助科研通管家采纳,获得10
22秒前
Owen应助科研通管家采纳,获得10
22秒前
SHIMMER应助科研通管家采纳,获得10
22秒前
田様应助科研通管家采纳,获得10
22秒前
小二郎应助科研通管家采纳,获得10
22秒前
22秒前
高分求助中
【此为提示信息,请勿应助】请按要求发布求助,避免被关 20000
ISCN 2024 – An International System for Human Cytogenomic Nomenclature (2024) 3000
Continuum Thermodynamics and Material Modelling 2000
Encyclopedia of Geology (2nd Edition) 2000
105th Edition CRC Handbook of Chemistry and Physics 1600
Maneuvering of a Damaged Navy Combatant 650
China—Art—Modernity: A Critical Introduction to Chinese Visual Expression from the Beginning of the Twentieth Century to the Present Day 360
热门求助领域 (近24小时)
化学 材料科学 医学 生物 工程类 有机化学 物理 生物化学 纳米技术 计算机科学 化学工程 内科学 复合材料 物理化学 电极 遗传学 量子力学 基因 冶金 催化作用
热门帖子
关注 科研通微信公众号,转发送积分 3776855
求助须知:如何正确求助?哪些是违规求助? 3322276
关于积分的说明 10209617
捐赠科研通 3037624
什么是DOI,文献DOI怎么找? 1666792
邀请新用户注册赠送积分活动 797656
科研通“疑难数据库(出版商)”最低求助积分说明 757976