Current understanding of IgA antibodies in the pathogenesis of IgA nephropathy

免疫学 肾病 免疫球蛋白A 抗体 肾小球肾炎 发病机制 同型 肾炎 分泌成分 补体系统 生物 免疫球蛋白G 医学 单克隆抗体 内分泌学 糖尿病
作者
Yasunori Nihei,Hitoshi Suzuki,Yusuke Suzuki
出处
期刊:Frontiers in Immunology [Frontiers Media]
卷期号:14 被引量:4
标识
DOI:10.3389/fimmu.2023.1165394
摘要

Immunoglobulin A (IgA) is the most abundant isotype of antibodies, provides a first line of defense at mucosal surfaces against pathogens, and thereby contributes to mucosal homeostasis. IgA is generally considered as a non-inflammatory antibody because of its main function, neutralizing pathogenic virus or bacteria. Meanwhile, IgA can induce IgA-mediated diseases, such as IgA nephropathy (IgAN) and IgA vasculitis. IgAN is characterized by the deposition of IgA and complement C3, often with IgG and/or IgM, in the glomerular mesangial region, followed by mesangial cell proliferation and excessive synthesis of extracellular matrix in glomeruli. Almost half a century has passed since the first report of patients with IgAN; it remains debatable about the mechanism how IgA antibodies selectively bind to mesangial region—a hallmark of IgAN—and cause glomerular injuries in IgAN. Previous lectin- and mass-spectrometry-based analysis have revealed that IgAN patients showed elevated serum level of undergalactosylated IgA1 in O-linked glycans of its hinge region, called galactose-deficient IgA1 (Gd-IgA1). Thereafter, numerous studies have confirmed that the glomerular IgA from IgAN patients are enriched with Gd-IgA1; thus, the first hit of the current pathogenesis of IgAN has been considered to increase circulating levels of Gd-IgA1. Recent studies, however, demonstrated that this aberrant glycosylation alone is not sufficient to disease onset and progression, suggesting that several additional factors are required for the selective deposition of IgA in the mesangial region and induce nephritis. Herein, we discuss the current understanding of the characteristics of pathogenic IgA and its mechanism of inducing inflammation in IgAN.

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
lu_zhqi发布了新的文献求助10
刚刚
科研通AI6.4应助LiChen采纳,获得10
1秒前
kk关注了科研通微信公众号
3秒前
qqa发布了新的文献求助10
3秒前
歪歪歪打正着完成签到 ,获得积分10
3秒前
4秒前
柴磊发布了新的文献求助10
4秒前
Reborn完成签到,获得积分10
4秒前
5552222发布了新的文献求助10
4秒前
5秒前
5秒前
5秒前
5秒前
6秒前
咕噜咕噜发布了新的文献求助10
6秒前
Iva发布了新的文献求助10
6秒前
molihuakai应助酷酷的臻采纳,获得10
6秒前
7秒前
qiangxu完成签到,获得积分10
7秒前
stable完成签到,获得积分10
7秒前
宁宁关注了科研通微信公众号
7秒前
大王完成签到,获得积分10
7秒前
尊敬忆山发布了新的文献求助10
7秒前
JoJo完成签到,获得积分10
8秒前
8秒前
peekaboo完成签到,获得积分10
8秒前
9秒前
自在的榛子应助dx3906采纳,获得10
9秒前
完美世界应助zjl采纳,获得10
9秒前
10秒前
六六发布了新的文献求助10
10秒前
huanhuan发布了新的文献求助10
10秒前
stable发布了新的文献求助30
10秒前
wzx完成签到,获得积分10
10秒前
找呀找完成签到,获得积分10
11秒前
活泼的翅膀完成签到 ,获得积分20
11秒前
11秒前
七楼完成签到,获得积分10
12秒前
12秒前
struggle发布了新的文献求助10
12秒前
高分求助中
Principles of Economics, 11th Edition 10000
University Physics with Modern Physics, 16th edition 10000
(应助此贴封号)【重要!!请各用户(尤其是新用户)详细阅读】【科研通的精品贴汇总】 10000
Development of a Bridge Weigh-In-Motion System: A technology to convert the bridge response to the passage of traffic into data on vehicle configurations, speeds, times of travel and weights 1000
ズームレンズの光学設計に関する研究 800
Fundamentals of Pharmaceutical and Biologics Regulations: A Global Perspective, Second Edition 700
Matrix Methods in Data Mining and Pattern Recognition Second Edition 610
热门求助领域 (近24小时)
化学 材料科学 医学 生物 纳米技术 工程类 有机化学 化学工程 生物化学 计算机科学 内科学 物理 复合材料 催化作用 细胞生物学 无机化学 光电子学 物理化学 电极 基因
热门帖子
关注 科研通微信公众号,转发送积分 7283268
求助须知:如何正确求助?哪些是违规求助? 8904145
关于积分的说明 18838791
捐赠科研通 6953877
什么是DOI,文献DOI怎么找? 3207699
关于科研通互助平台的介绍 2377912
邀请新用户注册赠送积分活动 2182977