KATOU Hidehito
Department School of Medicine, School of Medicine Position |
|
Article types | Review article |
Language | Japanese |
Peer review | Peer reviewed |
Presence of invitation | Invited paper |
Title | What is inflammation. |
Journal | Formal name:Journal of Tokyo Women's Medical University Abbreviation:東女医大誌 ISSN code:00409022 |
Domestic / Foregin | Domestic |
Volume, Issue, Page | pp.1-13 |
Total page number | 13 |
Author and coauthor | Hidehito KATO |
Authorship | Lead author |
Publication date | 2020/02/15 |
Summary | Stress response is an important system for maintaining the homeostasis of a living organisms. After acute inflammation occurs, if tissue repair is incomplete, or if stress is not completely removed and an excessive inflammatory response is prolonged, damage is accumulated in living organ and chronic inflammation persists. As a result, irreversible tissue / organ damage accompanied by fibrosis occurs. Inflammatory diseases such as fibrotic diseases, autoimmune diseases, allergies, and arteriosclerosis account for most of the causes of death in humans, so it is extremely important to understand the mechanism of inflammation and establish its control method. Inflammation is caused by a complex influence of various molecules and cells that form networks through inflammatory cytokines. Because various factors influence each other, it is thought that the onset time, degree, and duration will differ. Therefore, there are many unknown factors. This article enumerates the innate immune system receptors (pattern recognition receptors) and responsible cells (Neutrophils, Innate Lymphoid Cells, natural killer T cells) that cause inflammation, explains the mechanism of inflammation, and presents findings on its regulatory factors and methods. The purpose of this article is to understand complex networks in inflammation. |
DOI | 10.24488 |