Kyoto University · Medicine
Professor Hiroshi Kawamoto's research lab focuses on molecular mechanisms underlying hematopoietic lineage commitment, particularly in T cell development and the regulation of innate lymphoid cell subsets such as invariant natural killer T (iNKT) cells. The lab investigates signaling pathways, transcriptional regulation, and post-transcriptional control mechanisms—such as those mediated by small non-coding RNAs like SgrS—in cellular stress responses and immune cell fate decisions. A key area of interest is the role of cytokines and Notch signaling in maintaining multipotency or driving lineage specification in hematopoietic progenitors. The lab also explores the development and function of distinct iNKT cell subpopulations defined by surface markers like IL-17RB and CD4, contributing to understanding immune homeostasis and type 2 immunity.
Figures are computed from collected data and may differ slightly.
In early T cell development, progenitors retaining the potential to generate myeloid and natural killer lineages are eventually determined to a specific T cell lineage. The molecular mechanisms that drive this determination step remain unclarified. We show that, when murine hematopoietic progenitors were cultured on immobilized Notch ligand DLL4 protein in the presence of a cocktail of cytokines including interleukin-7, progenitors developing toward T cells were arrested and the arrested cells e
SgrS is an Hfq-binding small antisense RNA that is induced upon phosphosugar stress. It forms a ribonucleoprotein complex with RNase E through Hfq to mediate silencing of the target ptsG mRNA encoding the membrane component of the glucose-specific phosphoenolpyruvate phosphotransferase system. Although SgrS is believed to act on ptsG mRNA through base pairing between complementary regions, this was not previously tested experimentally. We addressed the question of whether SgrS indeed forms an RN
ADVERTISEMENT RETURN TO ISSUELetterNEXTDiscovery of the First Potent and Selective Small Molecule Opioid Receptor-like (ORL1) Antagonist: 1-[(3R,4R)-1-Cyclooctylmethyl-3- hydroxymethyl-4-piperidyl]-3-ethyl- 1,3-dihydro-2H-benzimidazol-2-one (J-113397)Hiroshi Kawamoto, Satoshi Ozaki, Yoshiki Itoh, Mitsuru Miyaji, Sachie Arai, Hiroshi Nakashima, Tetsuya Kato, Hisashi Ohta, and Yoshikazu IwasawaView Author Information Banyu Tsukuba Research Institute in collaboration with Merck Research Laboratorie
There is heterogeneity in invariant natural killer T (iNKT) cells based on the expression of CD4 and the IL-17 receptor B (IL-17RB), a receptor for IL-25 which is a key factor in T(H)2 immunity. However, the development pathway and precise function of these iNKT cell subtypes remain unknown. IL-17RB⁺iNKT cells are present in the thymic CD44⁺/⁻ NK1.1⁻ population and develop normally even in the absence of IL-15, which is required for maturation and homeostasis of IL-17RB⁻iNKT cells producing IFN-
We established an experimental system in vitro to examine the developmental capacity of individual hematopoietic progenitors to generate T, B and myeloid (M) cells. By using this system we analyzed the process of lineage commitment of hematopoietic progenitors in murine fetal liver (FL). It is known that small numbers of B and M cells, in addition to T cells, are generated in a co-culture of hematopoietic progenitors and a deoxyguanosine-treated fetal thymus (FT) lobe. We tried to enhance the gr
Accumulation of phosphosugars such as glucose-6-phosphate causes a rapid degradation of ptsG mRNA encoding the major glucose transporter IICB(Glc) in an RNase E/degradosome-dependent manner. The destabilization of ptsG mRNA is caused by a small antisense RNA (SgrS) that is induced by phosphosugar stress. In this study, we analyzed a series of ptsG-crp translational fusions to identify the mRNA region required for the rapid degradation of ptsG mRNA. We found that the ptsG-crp mRNA is destabilized
Although adoptive transfer of cytotoxic T lymphocytes (CTL) offer a promising cancer therapeutic direction, the generation of antigen-specific CTL from patients has faced difficulty in efficient expansion in ex vivo culture. To resolve this issue, several groups have proposed that induced pluripotent stem cell technology be applied for the expansion of antigen-specific CTL, which retain expression of the same T-cell receptor as original CTL. However, in these previous studies, the regenerated CT
The most immature population of fetal thymus (FT) cells has been shown to generate not only T but also B and myeloid cells. The present study was undertaken to clarify whether such a multipotent activity of the earliest population of FT cells is attributed to multipotent hemopoietic progenitors or to a mixture of lineage-restricted progenitors. Examination of individual FT progenitors by a recently established clonal assay system, which is able to determine the developmental potential of each pr
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