The University of Osaka · Medicine
Professor Hyota Takamatsu's research lab focuses on innate immune signaling, particularly the molecular mechanisms underlying inflammasome activation and its role in sterile and infectious inflammatory diseases. The lab investigates how subcellular organelles, especially lysosomes, regulate immune responses through scaffolding complexes such as Ragulator, with a strong emphasis on NLRP3 inflammasome dynamics. They also explore biomarker discovery in autoimmune diseases, particularly lupus nephritis, by assessing bioactive forms of molecules like BAFF and type I interferons. Their work bridges basic immunology with translational applications in inflammatory and autoimmune disorders.
Figures are computed from collected data and may differ slightly.
The cellular activation of the NLRP3 inflammasome is spatiotemporally orchestrated by various organelles, but whether lysosomes contribute to this process remains unclear. Here, we show the vital role of the lysosomal membrane-tethered Ragulator complex in NLRP3 inflammasome activation. Deficiency of Lamtor1, an essential component of the Ragulator complex, abrogated NLRP3 inflammasome activation in murine macrophages and human monocytic cells. Myeloid-specific Lamtor1-deficient mice showed mark
Monitoring urinary BAFF-bioactivity may be valuable in diagnosing LN. Furthermore, stratification based on serum BAFF and IFN-I bioactivities may allow the identification of appropriate patients for biologics targeting BAFF and IFN-I.
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