| First Author | Ichikawa T | Year | 2019 |
| Journal | Nat Immunol | Volume | 20 |
| Issue | 11 | Pages | 1469-1480 |
| PubMed ID | 31591568 | Mgi Jnum | J:306326 |
| Mgi Id | MGI:6706618 | Doi | 10.1038/s41590-019-0494-y |
| Citation | Ichikawa T, et al. (2019) CD103(hi) Treg cells constrain lung fibrosis induced by CD103(lo) tissue-resident pathogenic CD4 T cells. Nat Immunol 20(11):1469-1480 |
| abstractText | Tissue-resident memory T cells (TRM cells) are crucial mediators of adaptive immunity in nonlymphoid tissues. However, the functional heterogeneity and pathogenic roles of CD4(+) TRM cells that reside within chronic inflammatory lesions remain unknown. We found that CD69(hi)CD103(lo) CD4(+) TRM cells produced effector cytokines and promoted the inflammation and fibrotic responses induced by chronic exposure to Aspergillus fumigatus. Simultaneously, immunosuppressive CD69(hi)CD103(hi)Foxp3(+) CD4(+) regulatory T cells were induced and constrained the ability of pathogenic CD103(lo) TRM cells to cause fibrosis. Thus, lung tissue-resident CD4(+) T cells play crucial roles in the pathology of chronic lung inflammation, and CD103 expression defines pathogenic effector and immunosuppressive tissue-resident cell subpopulations in the inflamed lung. |
