-
Categories
-
Pharmaceutical Intermediates
-
Active Pharmaceutical Ingredients
-
Food Additives
- Industrial Coatings
- Agrochemicals
- Dyes and Pigments
- Surfactant
- Flavors and Fragrances
- Chemical Reagents
- Catalyst and Auxiliary
- Natural Products
- Inorganic Chemistry
-
Organic Chemistry
-
Biochemical Engineering
- Analytical Chemistry
- Cosmetic Ingredient
-
Pharmaceutical Intermediates
Promotion
ECHEMI Mall
Wholesale
Weekly Price
Exhibition
News
-
Trade Service
Editor | xi Immune recognition is the core scientific issue of immunological research
.
The innate immune recognition receptor can recognize the endogenous "danger signals" caused by pathogenic microbial infections, tissue damage or internal environmental imbalance, so as to quickly initiate innate immunity and inflammatory response, thus in immune defense, immune homeostasis, and inflammatory diseases.
Play a key role
in the
In recent years, the research on the innate immune recognition mechanism of pathogenic microorganisms has made great progress.
At present, more than 50 innate immune recognition receptors have been discovered, such as Toll-like receptors, RIG-like receptors, NOD-like receptors, cGAS and so on
.
In addition to pathogenic microorganisms, innate immune cells can also recognize endogenous "danger signals" produced in the process of tissue damage and metabolic abnormalities, but the recognition mechanism is still unclear.
Only a few dangerous recognition receptors such as NLRP3 have been found.
.
Type 3 innate lymphoid cells (ILC3s) are innate immune cells discovered in recent years, mainly located in mucosal tissues
.
ILC3s can promote the proliferation and repair of epithelial cells by producing IL-22, and thus play a key role in maintaining the homeostasis of mucosal tissues such as the intestine and skin
.
Past studies have shown that in the process of tissue damage, ILC3s can be activated by cytokines, microbial metabolites, neuron signaling molecules, etc.
, but it has not been clear whether ILC3s can directly recognize tissue/cell damage
.
On June 8, 2021, the team of Professor Rongbin Zhou/Professor Wei Jiang from the University of Science and Technology of China published a research paper titled GPR34-mediated sensing of lysophosphatidylserine released by apoptotic neutrophils activates type 3 innate lymphoid cells to mediate tissue repair in Immunity, the first to prove that ILC3s can be used.
Directly identify tissue damage and find that GPR34 plays a key role in it
.
Using a model of colon injury induced by dextran sodium sulfate (DSS), researchers found that clearing neutrophils would lead to increased intestinal damage and weakened repair in mice
.
Mechanism studies have found that the activation of ILC3s cells in the mouse colon tissue and the production of IL-22 are weakened after neutrophils are cleared, and IL-22 supplementation can restore DSS-induced colon damage, indicating that neutrophils mediated during colon damage The activation of ILC3s
.
To further explore how neutrophils activate ILC3s, using in vitro co-culture and metabolomics analysis, the researchers found that apoptotic neutrophils can induce ILC3s activation and IL-22 by releasing lysophosphatidylserine (LysoPS) Produced
.
Further using gene-deficient mice and small molecule antagonists, the researchers proved that apoptotic neutrophils and LysoPS promote the activation of ILC3s by activating the G protein receptor GPR34 expressed by ILC3s
.
To further explore the role of GPR34 in tissue repair, the researchers used Gpr34 whole body knockout mice and ILC3s conditional knockout mice to prove that GPR34 plays a role in ILC3s activation, IL-22 production and tissue repair in colon and skin injury models.
Important role
.
The study was highly praised by the reviewers, who believed that the work “show for the first time that ILC3 can sense DAMPs” and “discovered a new activation method of ILC3s (a new way in which ILC3 are activated via DAMPs)”
.
In short, the innovation of this study is reflected in: (1) It is the first time that type III innate lymphocytes can directly recognize tissue damage; (2) It is found that GPR34 is a new risk recognition receptor; (3) It is suggested that GPR34 can be used as a treatment for inflammation.
Potential intervention targets for sexual bowel disease and skin inflammation
.
Wang Xiaqiong, postdoctoral fellow of the University of Science and Technology of China, and doctoral candidates Cai Juan and Lin Bolong are the co-first authors of the paper
.
Original link: https://doi.
org/10.
1016/j.
immuni.
2021.
05.
007 Plate maker: Notes for reprinting on the 11th [Non-original article] The copyright of this article belongs to the author of the article.
Personal forwarding and sharing are welcome.
Reprinting without permission is prohibited.
The author has all legal rights, and offenders must be investigated
.
.
The innate immune recognition receptor can recognize the endogenous "danger signals" caused by pathogenic microbial infections, tissue damage or internal environmental imbalance, so as to quickly initiate innate immunity and inflammatory response, thus in immune defense, immune homeostasis, and inflammatory diseases.
Play a key role
in the
In recent years, the research on the innate immune recognition mechanism of pathogenic microorganisms has made great progress.
At present, more than 50 innate immune recognition receptors have been discovered, such as Toll-like receptors, RIG-like receptors, NOD-like receptors, cGAS and so on
.
In addition to pathogenic microorganisms, innate immune cells can also recognize endogenous "danger signals" produced in the process of tissue damage and metabolic abnormalities, but the recognition mechanism is still unclear.
Only a few dangerous recognition receptors such as NLRP3 have been found.
.
Type 3 innate lymphoid cells (ILC3s) are innate immune cells discovered in recent years, mainly located in mucosal tissues
.
ILC3s can promote the proliferation and repair of epithelial cells by producing IL-22, and thus play a key role in maintaining the homeostasis of mucosal tissues such as the intestine and skin
.
Past studies have shown that in the process of tissue damage, ILC3s can be activated by cytokines, microbial metabolites, neuron signaling molecules, etc.
, but it has not been clear whether ILC3s can directly recognize tissue/cell damage
.
On June 8, 2021, the team of Professor Rongbin Zhou/Professor Wei Jiang from the University of Science and Technology of China published a research paper titled GPR34-mediated sensing of lysophosphatidylserine released by apoptotic neutrophils activates type 3 innate lymphoid cells to mediate tissue repair in Immunity, the first to prove that ILC3s can be used.
Directly identify tissue damage and find that GPR34 plays a key role in it
.
Using a model of colon injury induced by dextran sodium sulfate (DSS), researchers found that clearing neutrophils would lead to increased intestinal damage and weakened repair in mice
.
Mechanism studies have found that the activation of ILC3s cells in the mouse colon tissue and the production of IL-22 are weakened after neutrophils are cleared, and IL-22 supplementation can restore DSS-induced colon damage, indicating that neutrophils mediated during colon damage The activation of ILC3s
.
To further explore how neutrophils activate ILC3s, using in vitro co-culture and metabolomics analysis, the researchers found that apoptotic neutrophils can induce ILC3s activation and IL-22 by releasing lysophosphatidylserine (LysoPS) Produced
.
Further using gene-deficient mice and small molecule antagonists, the researchers proved that apoptotic neutrophils and LysoPS promote the activation of ILC3s by activating the G protein receptor GPR34 expressed by ILC3s
.
To further explore the role of GPR34 in tissue repair, the researchers used Gpr34 whole body knockout mice and ILC3s conditional knockout mice to prove that GPR34 plays a role in ILC3s activation, IL-22 production and tissue repair in colon and skin injury models.
Important role
.
The study was highly praised by the reviewers, who believed that the work “show for the first time that ILC3 can sense DAMPs” and “discovered a new activation method of ILC3s (a new way in which ILC3 are activated via DAMPs)”
.
In short, the innovation of this study is reflected in: (1) It is the first time that type III innate lymphocytes can directly recognize tissue damage; (2) It is found that GPR34 is a new risk recognition receptor; (3) It is suggested that GPR34 can be used as a treatment for inflammation.
Potential intervention targets for sexual bowel disease and skin inflammation
.
Wang Xiaqiong, postdoctoral fellow of the University of Science and Technology of China, and doctoral candidates Cai Juan and Lin Bolong are the co-first authors of the paper
.
Original link: https://doi.
org/10.
1016/j.
immuni.
2021.
05.
007 Plate maker: Notes for reprinting on the 11th [Non-original article] The copyright of this article belongs to the author of the article.
Personal forwarding and sharing are welcome.
Reprinting without permission is prohibited.
The author has all legal rights, and offenders must be investigated
.
