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Background <p>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.</p> Methods <p>Spatial transcriptomics was performed on FFPE samples from lymph nodes of three CD patients with different histologic types and one normal lymph node.</p> Results <p>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.</p> Conclusions <p>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.</p>

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Spatial transcriptomics study of Castleman disease

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年4月19日

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  • Yanfang Chen,
  • Zhe Zhang,
  • Ling Li,
  • Mingzhi Zhang,
  • Zhaoming Li

摘要

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.