Toll-like receptor expression during inflammatory processes in human diseases

被引:0
|
作者
Dhakad, Prashant K. [1 ]
Mishra, Raghav [2 ]
Mishra, Isha [3 ]
机构
[1] Suresh Gyan Vihar Univ, Gyan Vihar Sch Pharm, Dept Pharmacol, Jaipur 302017, Rajasthan, India
[2] Lloyd Inst Management & Technol, Greater Noida, Uttar Pradesh, India
[3] Galgotias Coll Pharm, Greater Noida, Uttar Pradesh, India
来源
RHEUMATOLOGY & AUTOIMMUNITY | 2025年 / 5卷 / 01期
关键词
diseases; immunological reaction; ligands; signaling pathways; Toll-like receptor; AGONIST; RECOGNITION; MECHANISMS; INFECTION; NECROSIS; IMMUNITY; HEALTH; TLRS;
D O I
10.1002/rai2.12167
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Multi-cellular organisms, including humans, have evolved immune systems as defense mechanisms against pathogens. The immune system employs the Toll-like receptor (TLR) family as its primary defensive mechanism against infections. Their capacity to identify both foreign microbes and endogenous substances renders them crucial for controlling immune responses. This article aims to provide an overview of the structure, functions, properties and signaling mechanisms of TLRs. Additionally, it explores the involvement of TLRs in various disorders and discusses therapeutic strategies targeting TLR signaling pathways. TLRs are widely present in immune and non-immune cells and are dynamically regulated based on specific stimuli, such as pathogens or damaged host cells. Their activation triggers signaling cascades that lead to the production of type 1 interferons and proinflammatory cytokines. However, excessive TLR activation disrupts immune homeostasis and contributes to inflammatory and autoimmune diseases. Innovative TLR signaling pathway antagonists and inhibitors have been developed to combat these conditions. TLRs are central to the immune system's ability to combat infections and maintain natural defenses. A novel challenge in the treatment of numerous disorders is the preservation of immune homeostasis while targeting TLR signaling.
引用
收藏
页码:1 / 14
页数:14
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