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Status |
Public on Oct 12, 2024 |
Title |
Autoimmune CD4 T cells maintain function and survive in chronic autoimmunity by restricting terminal differentiation |
Organism |
Mus musculus |
Experiment type |
Expression profiling by high throughput sequencing Genome binding/occupancy profiling by high throughput sequencing
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Summary |
The mechanisms behind survival of autoimmune CD4 T cells during chronic stimulation are unclear. Examining early time-points during T cell priming showed that activation of autoimmune CD4 T cells in the absence of infectious signals allowed maintenance of TCF1 expression, albeit at reduced levels. Tcf7 locus was epigenetically modified in circulating autoimmune CD4 T cells, suggesting a pre-programmed de novo methylation of the locus in early stages of autoimmune CD4 T cell differentiation which mirrored the epigenetic profile of recently recruited CD4 CD62L+ T cells in the tissue. Collectively, the data presented here show that the unique environment during autoimmune CD4 T cell priming allows T cells to finetune TCF1 expression to maintain long-term survival and function.
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Overall design |
pancreatic islets, spleen+non-draining lymph nodes were harvested from BDC2.5 transferred cells into congenically labelled NOD mice. BDC2.5 CD4+Vb4 cells were sorted and subjected to 10X multiome scATAC/Gene expression sequncing
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Contributor(s) |
Aljobaily N, Allard D, Perkins B, Raugh A, Galland T, Jing Y, Stephens W, Bettini ML, Hale J, Bettini M |
Citation missing |
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Submission date |
Jul 19, 2024 |
Last update date |
Oct 12, 2024 |
Contact name |
Maria Bettini |
E-mail(s) |
Maria.Bettini@path.utah.edu
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Organization name |
University of Utah
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Department |
Pathology
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Lab |
Maria Bettini
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Street address |
University of Utah
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City |
Salt Lake City |
State/province |
Utah |
ZIP/Postal code |
84112 |
Country |
USA |
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Platforms (1) |
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Samples (4)
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GSM8408783 |
ATAC pancreatic islet CD4 BDC2.5 T cells |
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Relations |
BioProject |
PRJNA1137917 |