Emerging roles of IL-34 in neurodegenerative and neurological infectious disease

免疫学 医学 炎症 疾病 多发性硬化 免疫失调 免疫系统 病理
作者
Gaurav Chhetri
出处
期刊:International Journal of Neuroscience [Informa]
卷期号:133 (6): 660-671 被引量:3
标识
DOI:10.1080/00207454.2021.1963962
摘要

Neurological infections are often devastating in their clinical presentation. Although significant advances have made in neuroimaging techniques and molecular tools for diagnosis, as well as in anti-infective therapy, these diseases always difficult to diagnose and treat. Neuroparasitic infections and virus infections lead to neurological infections. In the nervous system, various cytokines and chemokines act as neuroinflammatory agents, neuromodulators, regulate neurodevelopment, and synaptic transmission. Among the most important cytokines, interleukins (ILs) are a large group of immunomodulatory proteins that elicit a wide variety of responses in cells and tissues. These ILs are involved in pro and anti-inflammatory effects, systemic inflammation, immune system modulation and play crucial roles in fighting cancer, infectious disease, and neurological disorders. Interleukin-34 (IL-34) identified by screening a comprehensive human protein library containing ∼3400 secreted and extracellular domain proteins in a human monocyte viability assay. Recent evidence has disclosed the crucial roles of IL-34 in the proliferation and differentiation of mononuclear phagocyte lineage cells, osteoclastogenesis, and inflammation. Additionally, IL-34 plays an important role in development, homeostasis, and disease. Dysregulation in IL-34 function can lead to various inflammatory and infectious diseases (e.g. Inflammatory bowel disease, liver fibrosis, Systemic Lupus erythematosus, rheumatoid arthritis), neurological disorders (e.g. Alzheimer disease) and neurological infectious disease (e.g. West Nile virus disease). In this review, we explore the biological role of IL-34 in addition to various impairments caused by dysregulation in IL-34 and discuss their potential links that may lead to important therapeutic and/or preventive strategies for these disorders.

科研通智能强力驱动
Strongly Powered by AbleSci AI
更新
大幅提高文件上传限制,最高150M (2024-4-1)

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
SciGPT应助seusyy采纳,获得10
刚刚
星威发布了新的文献求助10
刚刚
1秒前
blue完成签到 ,获得积分10
2秒前
今后应助yyy采纳,获得10
2秒前
自由冬亦发布了新的文献求助10
3秒前
如意新晴完成签到,获得积分10
3秒前
SciGPT应助罗燕采纳,获得10
3秒前
方向完成签到 ,获得积分10
3秒前
4秒前
aacc956完成签到 ,获得积分10
4秒前
千年老妖发布了新的文献求助10
4秒前
5秒前
zhang关注了科研通微信公众号
5秒前
乐乐乐乐乐乐应助LouieHuang采纳,获得10
6秒前
科研通AI2S应助文献打人采纳,获得10
7秒前
7秒前
ffff完成签到,获得积分10
7秒前
PSCs发布了新的文献求助10
7秒前
赘婿应助lisa采纳,获得10
8秒前
9秒前
10秒前
11秒前
FashionBoy应助科研通管家采纳,获得10
11秒前
11秒前
科研通AI2S应助科研通管家采纳,获得10
12秒前
完美世界应助科研通管家采纳,获得10
12秒前
tulips发布了新的文献求助10
12秒前
领导范儿应助科研通管家采纳,获得10
12秒前
大个应助科研通管家采纳,获得10
12秒前
CodeCraft应助科研通管家采纳,获得10
12秒前
英俊的铭应助科研通管家采纳,获得10
12秒前
coco应助科研通管家采纳,获得20
12秒前
Owen应助科研通管家采纳,获得10
12秒前
慕青应助科研通管家采纳,获得10
12秒前
田様应助科研通管家采纳,获得10
13秒前
斯文败类应助科研通管家采纳,获得10
13秒前
斯文败类应助科研通管家采纳,获得10
13秒前
英俊的铭应助科研通管家采纳,获得10
13秒前
Jasper应助科研通管家采纳,获得10
13秒前
高分求助中
歯科矯正学 第7版(或第5版) 1004
Smart but Scattered: The Revolutionary Executive Skills Approach to Helping Kids Reach Their Potential (第二版) 1000
Semiconductor Process Reliability in Practice 720
PraxisRatgeber: Mantiden: Faszinierende Lauerjäger 700
GROUP-THEORY AND POLARIZATION ALGEBRA 500
Mesopotamian divination texts : conversing with the gods : sources from the first millennium BCE 500
Days of Transition. The Parsi Death Rituals(2011) 500
热门求助领域 (近24小时)
化学 医学 生物 材料科学 工程类 有机化学 生物化学 物理 内科学 纳米技术 计算机科学 化学工程 复合材料 基因 遗传学 催化作用 物理化学 免疫学 量子力学 细胞生物学
热门帖子
关注 科研通微信公众号,转发送积分 3227367
求助须知:如何正确求助?哪些是违规求助? 2875446
关于积分的说明 8191043
捐赠科研通 2542695
什么是DOI,文献DOI怎么找? 1372977
科研通“疑难数据库(出版商)”最低求助积分说明 646618
邀请新用户注册赠送积分活动 621040