KLF2 Found to Steer S1PR1 and Control Memory CD8 T Cell Migration and Tissue Residency
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Research presented in an expert lecture on ImmuneZoom identifies the transcription factor KLF2 as a central regulator of memory CD8 T cell trafficking. KLF2 drives expression of S1PR1, the sphingosine-1-phosphate receptor 1, determining whether mature T cells exit the thymus and secondary lymphoid organs into blood circulation. CRISPR screens performed in P14 TCR transgenic mice during acute LCMV infection showed that KLF2 deficiency redistributes T cells, reducing their representation among small intestinal intraepithelial lymphocytes without inducing cell death, an effect partly compensated by S1PR5. KLF2 additionally regulates homing molecules including CXCR3 and L-selectin (CD62L). The findings bear on how tissue-resident memory T cell pools are maintained and have implications for PD-1 blockade strategies.
Written by a model from the reports · updated 2 hours ago
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- youtube.comKLF2 Drives S1PR1 to Control Memory CD8 T Cell Migration and Tissue Residency
An expert lecture on ImmuneZoom explains how the transcription factor KLF2 drives expression of S1PR1 (sphingosine-1-phosphate receptor 1), controlling whether mature T cells leave the thymus and secondary lymphoid organs to enter blood circulation. CRISPR screens in P14 TCR transgenic mice during acute LCMV infection showed that KLF2 deficiency shifts T cell distribution, reducing representation among small intestinal intraepithelial lymphocytes without causing cell death, partly compensated by S1PR5. KLF2 also regulates homing molecules such as CXCR3 and L-selectin (CD62L), informing work on tissue-resident memory T cell pools and PD-1 blockade.
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