Publications by authors named "Sonoko Tasaki"

Article Synopsis
  • Th17 cells play a crucial role in the immune response against oral pathogens, particularly in the development of periodontitis.
  • The oral pathobiont Porphyromonas gingivalis exacerbates periodontitis by promoting Th17 cell differentiation, which occurs in Peyer's patches and allows these cells to migrate to oral tissues.
  • The study shows that the intestinal microbiome influences Th17 cell response, with antibiotic treatment altering the microbiome potentially impacting the progression of periodontitis.
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Article Synopsis
  • Maternal immune activation (MIA) due to bacterial infection, specifically through lipopolysaccharide (LPS), can negatively impact fetal brain development and lead to autism spectrum disorder (ASD)-like behaviors in mouse offspring.
  • This study shows that LPS exposure triggers an immune response marked by increased IL-17A levels and changes in immune cell activity both in the mother and the fetal brain.
  • Blocking IL-17A in the context of LPS-induced MIA helped reduce the ASD-like behaviors in the offspring, highlighting the importance of the IL-17A pathway in this process.
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We previously reported that Candida albicans responded to mild heat stress in a range of temperature elevations simulating fever, and concluded that mild heat stress increases susceptibility to antifungal drugs. In this study, we show that mild heat stress causes a morphological change in hyphae during the process of biofilm formation. We found that mild heat stress extended the period of hyphal stage maintenance in C.

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Candida albicans is a human commensal that causes opportunistic infections. Th17 cells provide resistance against mucosal infection with C. albicans; however, the T cell antigens remain little known.

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Activation of naive CD4 T cells results in the development of several distinct subsets of effector Th cells, including Th2 cells that play a pivotal role in allergic inflammation and helminthic infections. SWAP-70-like adapter of T cells (SLAT), also known as Def6 or IBP, is a guanine nucleotide exchange factor for small GTPases, which regulates CD4 T cell inflammatory responses by controlling Ca/NFAT signaling. In this study, we have identified a novel alternatively spliced isoform of SLAT, named SLAT2, which lacks the region encoded by exons 2-7 of the gene.

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