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TRPM5 Negatively Regulates Lipopolysaccharide-Induced Ca2+ Signaling of B Lymphocytes

ABSTRACT: TRPM5 Negatively Regulates Lipopolysaccharide-Induced Ca2+ Signaling of B Lymphocytes

PROVIDER: PRJNA555419 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9700090.fastq.gz	Fastqsanger.gz
	SRR9700091.fastq.gz	Fastqsanger.gz
	SRR9700082.fastq.gz	Fastqsanger.gz
	SRR9700092.fastq.gz	Fastqsanger.gz
	SRR9700083.fastq.gz	Fastqsanger.gz

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TRPM5 Negatively Regulates Lipopolysaccharide-Induced Ca2+ Signaling of B Lymphocytes

Project description:Ca2+ signaling cascades are essential for various immune cell functions. As such, most cells have negative regulators of Ca2+ homeostasis that strictly regulate cytosolic Ca2+ concentration, such as Ca2+-activated monovalent cation channels (CAMs). Transient receptor potential melastatin-related 5 channel (TRPM5), a CAM, is expressed in B lymphocytes. However, its functional role in the immune system is poorly understood. Here, we show that TRPM5 negatively modulates Ca2+ influx, thereby regulating lipopolysaccharide (LPS)-induced proliferative and inflammatory responses by B cells. Trpm5-deficient mice exhibited increased Ca2+ influx, enhanced proliferative responses, and increased production of inflammatory cytokines interleukin-6 and CXCL10 in LPS-stimulated B cells. However, Ca2+ chelation reduced LPS-induced cytokine production by Trpm5-deficient B cells. Furthermore, Trpm5-deficient mice showed exacerbation of endotoxic shock with high mortality. Our findings demonstrate the importance of TRPM5-dependent regulatory mechanisms in LPS-induced Ca2+ signaling of splenic B cells.

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