Kyoto University · Medicine
Professor Takashi Nomura's research lab focuses on parasitology and immunology, with a central emphasis on understanding the molecular mechanisms of drug resistance in malaria parasites, particularly chloroquine resistance in *Plasmodium vivax* and related species. The lab investigates the role of *pfcrt* homologues in parasite drug resistance and explores the genetic and evolutionary basis of antimalarial resistance. Additionally, the lab examines immune dysregulation in inflammatory skin diseases such as atopic dermatitis, with a focus on T-cell subsets (Th1, Th2, Th17, and Treg cells) and their cytokine networks in disease pathogenesis and treatment response. The integration of parasitology, immunogenetics, and translational medicine defines the lab’s interdisciplinary approach to infectious and immune-mediated diseases.
Figures are computed from collected data and may differ slightly.
Chloroquine (CQ)-resistant Plasmodium vivax malaria was first reported 12 years ago, nearly 30 years after the recognition of CQ-resistant P. falciparum. Loss of CQ efficacy now poses a severe problem for the prevention and treatment of both diseases. Mutations in a digestive vacuole protein encoded by a 13-exon gene, pfcrt, were shown recently to have a central role in the CQ resistance (CQR) of P. falciparum. Whether mutations in pfcrt orthologues of other Plasmodium species are involved in CQ
To assess the prevalence and clinical significance of restless legs syndrome (RLS) in a Japanese population, we carried out a community-based survey in a rural area of Japan. We sent questionnaires requesting information on demographics, the Center for Epidemiological Studies Depression scale, the Short Form-8, the Pittsburgh Sleep Quality Index, the National Institutes of Health/International RLS Study Group (IRLSSG) consensus questionnaire, and the IRLSSG severity scale for RLS (IRLS) to 5,528
Atopic dermatitis (AD) is a common T-cell-mediated inflammatory disease of the skin. Signatures of AD are characterized by an impaired skin barrier, aberrant Th2-type cytokine production and intensive pruritus. Transcriptomic analysis, however, has revealed a heterogeneous pathogenesis and the co-existence of multiple cytokine axes of Th17, Th22 and Th1 types, especially in intrinsic (a subtype of AD without skin barrier impairment), pediatric and Asian types of AD. Furthermore, the therapeutic
Skin protects body from continual attack by microbial pathogens and environmental factors. Such barrier function of skin is achieved by multiple components including immune system, which is mainly regulated by lymphocytes. T lymphocytes (T cells) that express T cell receptor (TCR) α and β chains (αβT cells) control the strength and the type of immune response. CD4T cell population consists of helper T (Th) cell-subsets and immunosuppressive regulatory T (Treg) cells. Th1 cells produce IFN-γ and
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