Journal of translational medicine · 2025
Spatial transcriptomics study of Castleman disease.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Chen Yanfang, Zhang Zhe, Li Ling, Zhang Mingzhi, Li Zhaoming
Аннотация
BACKGROUND: Castleman Disease (CD) is a rare lymphoproliferative disorder of uncertain etiology, primarily characterized by painless lymphadenopathy. To further understand the possible pathogenesis of the disease, we utilized spatial transcriptomics to explore CD.
METHODS: Spatial transcriptomics was performed on FFPE samples from lymph nodes of three CD patients with different histologic types and one normal lymph node.
RESULTS: The sample was categorized by analysis into 14 clusters, including B cells, plasma cells, BECs, LECs, CD4 + T cells, CD8 + T cells, macrophages, monocytes, cycling cells, myofibroblasts, mDCs, NKCs, Tfh and NESCs. Our study showed that the lesion cells of CD might be B cells. In addition to this, we found that mesenchymal cells, especially myofibroblasts, play an important role in disease progression and there was a large heterogeneity of cellular communication between cell clusters in different histologic types of CD.
CONCLUSIONS: Through this study we have gained a better understanding of the pathogenesis of CD. It provides new ideas for the subsequent exploration of CD and directions for the development of new clinical drugs.
METHODS: Spatial transcriptomics was performed on FFPE samples from lymph nodes of three CD patients with different histologic types and one normal lymph node.
RESULTS: The sample was categorized by analysis into 14 clusters, including B cells, plasma cells, BECs, LECs, CD4 + T cells, CD8 + T cells, macrophages, monocytes, cycling cells, myofibroblasts, mDCs, NKCs, Tfh and NESCs. Our study showed that the lesion cells of CD might be B cells. In addition to this, we found that mesenchymal cells, especially myofibroblasts, play an important role in disease progression and there was a large heterogeneity of cellular communication between cell clusters in different histologic types of CD.
CONCLUSIONS: Through this study we have gained a better understanding of the pathogenesis of CD. It provides new ideas for the subsequent exploration of CD and directions for the development of new clinical drugs.