| First Author | Shin SM | Year | 2007 |
| Journal | J Leukoc Biol | Volume | 81 |
| Issue | 6 | Pages | 1455-65 |
| PubMed ID | 17389581 | Mgi Jnum | J:122336 |
| Mgi Id | MGI:3714089 | Doi | 10.1189/jlb.1006619 |
| Citation | Shin SM, et al. (2007) 4-1BB triggers IL-13 production from T cells to limit the polarized, Th1-mediated inflammation. J Leukoc Biol 81(6):1455-65 |
| abstractText | 4-1BB (CD137) triggering typically induces Th1 response by increasing IFN-gamma from T cells upon TCR ligation. We found recently that 4-1BB costimulation increased the expression of IL-13 from CD4(+) T cells, as well as CD8(+) T cells. The enhanced IL-13 expression by agonistic anti-4-1BB treatment was mediated via MAPK1/2, PI-3K, JNK, mammalian target of rapamycin, NF-AT, and NF-kappaB signaling pathways. The signaling for IL-13 induction was similar to that of IFN-gamma production by anti-4-1BB treatment in T cells. When the anti-4-1BB-mediated IL-13 expression was tested in an in vivo viral infection model such as HSV-1 and vesicular stomatitis virus, 4-1BB stimulation enhanced IL-13 expression of CD4(+) T, rather than CD8(+) T cells. Although IL-13 was enhanced by anti-4-1BB treatment, the increased IL-13 did not significantly alter the anti-4-1BB-induced Th1 polarization of T cells-increase of T-bet and decrease of GATA-3. Nevertheless, anti-4-1BB treatment polarized T cells excessively in the absence of IL-13 and even became detrimental to the mice by causing liver inflammation. Therefore, we concluded that IL-13 was coinduced following 4-1BB triggering to maintain the Th1/2 balance of immune response. |
