The CLICs family of intracerine ion channel proteins play an important role in the small body of NLRP3 inflammation.

Recently, Zhou Rongbin, professor of life sciences, microscale national laboratory (chip), medical center and key laboratory of natural immunity and chronic diseases of the Chinese Academy of Sciences, Jiang Wei Research Group, in cooperation with Wang Jun Research Group, Bai Li Research Group and Sun Yat-sen University Professor Cui Wei Research Group, revealed the important role of the CLICs family in the small body of intracerine chloride channel protein in NLRP3 inflammation.
the study was published August 4 in the journal Nature Communications.
inflammatory response is an important immune defense mechanism of the body, which helps the body to resist pathogenic microbial infection.
, inflammatory response disorders can also lead to tissue and organ damage, which can promote disease.
, chronic inflammatory responses are involved in the development of almost all major diseases in humans, so understanding the processes of inflammatory responses has the potential to provide new strategies for disease treatment.
NLRP3 inflammatory small body is a multiprotein complex consisting of intrinsic immune receptonin NLRP3 and downstream joint protein ASC and protease caspase-1 as the core, and its activity can promote the maturation and secretion of inflammatory factors such as IL-1b and IL-18, thus promoting the development of inflammatory response.
NLRP3 inflammatory small body has been reported in recent years to participate in the occurrence of type 2 diabetes, gout, Parkinson's, Alhaimer, fatty liver and other major human diseases, suggesting that NLRP3 inflammatory small body is a potential intervention target for these diseases.
therefore explore the active mechanism of NLRP3 inflammatory small body not only helps to understand the publishing mechanism of the above-mentioned diseases, but also provides potential treatment.
NLRP3 inflammatory small body can perceive a variety of red flags inside and outside the body, such as high blood sugar, high blood lipids, uric acid crystallization, cholesterol crystallization, etc. , but the above-mentioned red flag induced NLRP3 active molecular mechanism is not clear.
past work has shown that hazard signals can induce the loss of potassium ions and mitochondrial damage in cells, but how changes in potassium ions and mitochondrial damage induce subsequent inflammation of small body assembly molecular mechanisms have not been revealed.
the work found that the active oxygen produced by the CLICs protein family's online granulal damage could be induced to migrate to the cell membrane to mediat the flow of chlorine ions in the cell, thus further promoting the assembly of the NLRP3 inflammatory glycerin.
inhibit the expression or activity of the CLICs family protein can significantly inhibit the activity of NLRP3 inflammatory small body.
the work not only found that CLICs-mediated chloride ion exogenation was a key time in the upstream assembly of NLRP3 inflammatory bodies, but also suggested that CLICs could be targeted for NLRP3-related inflammatory diseases.
research has been supported by the Fund Committee, the Ministry of Science and Technology, the Central Group Department and the Chinese Academy of Sciences.
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