| First Author | Reynolds LA | Year | 2012 |
| Journal | J Immunol | Volume | 189 |
| Issue | 3 | Pages | 1113-7 |
| PubMed ID | 22753928 | Mgi Jnum | J:189778 |
| Mgi Id | MGI:5446984 | Doi | 10.4049/jimmunol.1200991 |
| Citation | Reynolds LA, et al. (2012) Cutting edge: in the absence of TGF-beta signaling in T cells, fewer CD103+ regulatory T cells develop, but exuberant IFN-gamma production renders mice more susceptible to helminth infection. J Immunol 189(3):1113-7 |
| abstractText | Multiple factors control susceptibility of C57BL/6 mice to infection with the helminth Heligmosomoides polygyrus, including TGF-beta signaling, which inhibits immunity in vivo. However, mice expressing a T cell-specific dominant-negative TGF-beta receptor II (TGF-betaRII DN) show dampened Th2 immunity and diminished resistance to infection. Interestingly, H. polygyrus-infected TGF-betaRII DN mice show greater frequencies of CD4(+)Foxp3(+)Helios(+) Tregs than infected wild-type mice, but levels of CD103 are greatly reduced on both these cells and on the CD4(+)Foxp3(+)Helios(-) population. Although Th9 and Th17 levels are comparable between infected TGF-betaRII DN and wild-type mice, the former develop exaggerated CD4(+) and CD8(+) T cell IFN-gamma responses. Increased susceptibility conferred by TGF-betaRII DN expression was lost in IFN-gamma-deficient mice, although they remained unable to completely clear infection. Hence, overexpression of IFN-gamma negatively modulates immunity, and the presence of Helios(+) Tregs may maintain susceptibility on the C57BL/6 background. |
