| First Author | Guo K | Year | 2024 |
| Journal | Sci Adv | Volume | 10 |
| Issue | 1 | Pages | eadj1120 |
| PubMed ID | 38170765 | Mgi Jnum | J:352246 |
| Mgi Id | MGI:7575271 | Doi | 10.1126/sciadv.adj1120 |
| Citation | Guo K, et al. (2024) The chemokine receptor CXCR3 promotes CD8(+) T cell-dependent lung pathology during influenza pathogenesis. Sci Adv 10(1):eadj1120 |
| abstractText | The dual role of CD8(+) T cells in influenza control and lung pathology is increasingly appreciated. To explore whether protective and pathological functions can be linked to specific subsets, we dissected CD8(+) T responses in influenza-infected murine lungs. Our single-cell RNA-sequencing (scRNA-seq) analysis revealed notable diversity in CD8(+) T subpopulations during peak viral load and infection-resolved state. While enrichment of a Cxcr3(hi) CD8(+) T effector subset was associated with a more robust cytotoxic response, both CD8(+) T effector and central memory exhibited equally potent effector potential. The scRNA-seq analysis identified unique regulons regulating the cytotoxic response in CD8(+) T cells. The late-stage CD8(+) T blockade in influenza-cleared lungs or continuous CXCR3 blockade mitigated lung injury without affecting viral clearance. Furthermore, adoptive transfer of wild-type CD8(+) T cells exacerbated influenza lung pathology in Cxcr3(-/-) mice. Collectively, our data imply that CXCR3 interception could have a therapeutic effect in preventing influenza-linked lung injury. |
