A review: Mechanisms and molecular pathways of signaling lymphocytic activation molecule family 3 (SLAMF3) in immune modulation and therapeutic prospects

免疫系统 生物 信号转导 自身免疫 背景(考古学) 免疫学 获得性免疫系统 神经科学 细胞生物学 古生物学
作者
Tong Zhou,Yanjie Guan,Lin Sun,Wentao Liu
出处
期刊:International Immunopharmacology [Elsevier BV]
卷期号:133: 112088-112088 被引量:4
标识
DOI:10.1016/j.intimp.2024.112088
摘要

The signaling lymphocytic activation molecule (SLAM) family participates in the modulation of various innate and adaptive immune responses. SLAM family (SLAMF) receptors include nine transmembrane glycoproteins, of which SLAMF3 (also known as CD229 or Ly9) has important roles in the modulation of immune responses, from the fundamental activation and suppression of immune cells to the regulation of intricate immune networks. SLAMF3 is mainly expressed in immune cells, such as T, B, and natural killer cells. It has a unique molecular structure, including four immunoglobulin-like domains in the extracellular domain and two immunoreceptor tyrosine-based signaling motifs in the intracellular structural domains. These unique structures have important implications for protein functioning. SLAMF3 is involved in pathogenesis of various disease, particularly autoimmune diseases and cancer. However, despite its potential clinical significance, a comprehensive overview of the current paradigm of SLAMF3 research is lacking. This review summarizes the structure, functional mechanisms, and therapeutic implications of SLAMF3. Our findings highlight the significance of SLAMF3 in both physiological and pathological contexts, and underline its dual role in autoimmunity and malignancies, and including disease progression and prognosis. The review also proposes that future studies on SLAMF3 should explore its context-specific inhibitory and stimulatory effects, expand on its potential in disease mapping, investigate related signaling pathways, and explore its value as a drug target. Research in these areas related to SLAMF3 can provide more precise directions for future therapeutic strategies.

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
wxf完成签到,获得积分10
8秒前
浩然完成签到 ,获得积分10
9秒前
9秒前
Mia完成签到 ,获得积分10
11秒前
如意的小鸭子完成签到 ,获得积分10
12秒前
12秒前
zhangj696完成签到,获得积分10
15秒前
趁热拿铁完成签到 ,获得积分10
16秒前
任性茉莉完成签到 ,获得积分10
17秒前
星空完成签到 ,获得积分10
19秒前
豆豆完成签到 ,获得积分10
20秒前
执念完成签到,获得积分10
21秒前
Double_N完成签到,获得积分10
24秒前
Chikit完成签到,获得积分10
26秒前
小张完成签到 ,获得积分10
30秒前
有魅力的藏鸟完成签到,获得积分10
31秒前
zuto吗喽完成签到,获得积分10
32秒前
Monroe完成签到 ,获得积分10
34秒前
蚂蚁飞飞完成签到,获得积分10
34秒前
Java完成签到,获得积分10
35秒前
桃枝气泡完成签到 ,获得积分10
38秒前
waveless完成签到,获得积分10
40秒前
SCI硬通货完成签到 ,获得积分10
45秒前
嘻嘻我完成签到,获得积分10
45秒前
优雅绮波完成签到 ,获得积分10
47秒前
weng完成签到,获得积分10
47秒前
47秒前
jing完成签到 ,获得积分10
52秒前
单小芫完成签到 ,获得积分10
52秒前
2012csc完成签到 ,获得积分0
52秒前
蜜果羹完成签到 ,获得积分10
52秒前
纯真的梦竹完成签到,获得积分10
53秒前
guiliang_x完成签到,获得积分10
54秒前
LMF完成签到 ,获得积分10
55秒前
平常的樱桃完成签到 ,获得积分10
58秒前
123完成签到,获得积分10
59秒前
无言发布了新的文献求助10
1分钟前
舒心冷珍完成签到 ,获得积分10
1分钟前
Kao应助科研通管家采纳,获得10
1分钟前
脑洞疼应助zihuan采纳,获得10
1分钟前
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
Organic Reactions, Volume 116 1000
Current concepts in cutaneous toxicity : proceedings of the Fourth Conference on Cutaneous Toxicity, Washington, D.C., May 9-11, 1979 1000
ズームレンズの光学設計に関する研究 800
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 7275375
求助须知:如何正确求助?哪些是违规求助? 8896518
关于积分的说明 18808229
捐赠科研通 6948235
什么是DOI,文献DOI怎么找? 3205767
关于科研通互助平台的介绍 2377289
邀请新用户注册赠送积分活动 2180565