TRPM5 Negatively Regulates Calcium-Dependent Responses in Lipopolysaccharide-Stimulated B Lymphocytes

Taiki Sakaguchi, Ryu Okumura, Chisato Ono, Daisuke Okuzaki, Takafumi Kawai, Yoshifumi Okochi, Natsuko Tanimura, Mari Murakami, Hisako Kayama, Eiji Umemoto, Hidetaka Kioka, Tomohito Ohtani, Yasushi Sakata, Kensuke Miyake, Yasushi Okamura, Yoshihiro Baba, Kiyoshi Takeda

Research output: Contribution to journalArticlepeer-review

7 Citations (Scopus)


B cells produce high amounts of cytokines and immunoglobulins in response to lipopolysaccharide (LPS) stimulation. Calcium signaling cascades are critically involved in cytokine production of T cells, and the cytosolic calcium concentration is regulated by calcium-activated monovalent cation channels (CAMs). Calcium signaling is also implicated in B cell activation; however, its involvement in the cytokine production of LPS-stimulated B cells remains less well characterized. Here, we show that the transient receptor potential melastatin 5 channel (TRPM5), which is one of the CAMs, negatively modulates calcium signaling, thereby regulating LPS-induced proliferative and inflammatory responses by B cells. LPS-stimulated B cells of Trpm5-deficient mice exhibit an increased cytosolic calcium concentration, leading to enhanced proliferation and the production of the inflammatory cytokines interleukin-6 and CXCL10. Furthermore, Trpm5-deficient mice show an exacerbation of endotoxic shock with high mortality. Our findings demonstrate the importance of TRPM5-dependent regulatory mechanisms in LPS-induced calcium signaling of splenic B cells.

Original languageEnglish
Article number107755
JournalCell Reports
Issue number10
Publication statusPublished - Jun 9 2020

All Science Journal Classification (ASJC) codes

  • Biochemistry, Genetics and Molecular Biology(all)


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