Single-cell transcriptomic characterization of microscopic colitis

Stefan Halvorsen, Molly Thomas, Mari Mino-Kenudson, Yuko Kinowaki, Kristin E. Burke, David Morgan, Kaia C. Miller, Katherine M. Williams, Jenny Gurung, Jessica McGoldrick, Megan Hopton, Brooke Hoppe, Nandini Samanta, Sidney Martin, Alice Tirard, Benjamin Y. Arnold, Jessica Tantivit, Joseph Yarze, Kyle Staller, Daniel C. Chung, Alexandra-Chloé Villani, Slim Sassi and Hamed Khalili ()
Additional contact information
Stefan Halvorsen: Massachusetts General Hospital (MGH)
Molly Thomas: MGH
Mari Mino-Kenudson: Harvard Medical School (HMS)
Yuko Kinowaki: MGH
Kristin E. Burke: MGH
David Morgan: MGH
Kaia C. Miller: MGH
Katherine M. Williams: MGH
Jenny Gurung: MGH
Jessica McGoldrick: MGH
Megan Hopton: Massachusetts General Hospital (MGH)
Brooke Hoppe: Massachusetts General Hospital (MGH)
Nandini Samanta: MGH
Sidney Martin: MGH
Alice Tirard: MGH
Benjamin Y. Arnold: MGH
Jessica Tantivit: MGH
Joseph Yarze: MGH
Kyle Staller: MGH
Daniel C. Chung: MGH
Alexandra-Chloé Villani: MGH
Slim Sassi: Massachusetts General Hospital (MGH)
Hamed Khalili: Broad Institute of Massachusetts Institute of Technology (MIT) and Harvard

Nature Communications, 2025, vol. 16, issue 1, 1-16

Abstract: Abstract Microscopic colitis (MC) is a chronic inflammatory disease of the large intestine and a common cause of chronic diarrhea in older adults. Here, we use single-cell RNA sequencing analysis of colonic mucosal tissue to build a cellular and molecular model for MC. Our results show that in MC, there is a substantial expansion of tissue CD8+ T cells, likely arising from local expansion following T cell receptor engagement. Within the T cell compartment, MC is characterized by a shift in CD8 tissue-resident memory T cells towards a highly cytotoxic and inflammatory phenotype and expansion of CD4+ T regulatory cells. These results provide insight into inflammatory cytokines shaping MC pathogenesis and highlight notable similarities and differences with other immune-mediated intestinal diseases, including a common upregulation of IL26 and an MC-specific upregulation of IL10. These data help identify targets against enteric T cell subsets as an effective strategy for treatment of MC.

Date: 2025
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Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:16:y:2025:i:1:d:10.1038_s41467-025-59648-8

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DOI: 10.1038/s41467-025-59648-8

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