AI Article Synopsis
- Tissue-resident memory T cells (specifically CD8 T cells) are crucial for quickly controlling infections in specific tissues, and their residency is influenced by the transcription factor Runx3.
- CD4 T cells, lacking Runx3, do not develop the necessary transcriptional network to maintain residency like CD8 T cells do, primarily due to the need for Runx1 and the minimal presence of Runx3.
- Introducing Runx3 into CD4 T cells activates the TGF-β transcriptional network, leading to improved survival, retention in tissues, redistribution towards epithelial areas, and better overall functionality.
Article Abstract
Tissue-resident memory T cells (T cells) provide rapid and superior control of localized infections. While the transcription factor Runx3 is a critical regulator of CD8 T cell tissue residency, its expression is repressed in CD4 T cells. Here, we show that, as a direct consequence of this Runx3-deficiency, CD4 T cells lacked the transforming growth factor (TGF)-β-responsive transcriptional network that underpins the tissue residency of epithelial CD8 T cells. While CD4 T cell formation required Runx1, this, along with the modest expression of Runx3 in CD4 T cells, was insufficient to engage the TGF-β-driven residency program. Ectopic expression of Runx3 in CD4 T cells incited this TGF-β-transcriptional network to promote prolonged survival, decreased tissue egress, a microanatomical redistribution towards epithelial layers and enhanced effector functionality. Thus, our results reveal distinct programming of tissue residency in CD8 and CD4 T cell subsets that is attributable to divergent Runx3 activity.
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| http://dx.doi.org/10.1038/s41590-022-01273-4 | DOI Listing |
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