| First Author | Hsu TL | Year | 2005 |
| Journal | J Immunol | Volume | 175 |
| Issue | 8 | Pages | 5135-45 |
| PubMed ID | 16210617 | Mgi Jnum | J:119121 |
| Mgi Id | MGI:3701193 | Doi | 10.4049/jimmunol.175.8.5135 |
| Citation | Hsu TL, et al. (2005) Attenuation of Th1 response in decoy receptor 3 transgenic mice. J Immunol 175(8):5135-45 |
| abstractText | The soluble decoy receptor 3 (DcR3) is a member of the TNFR superfamily. Because DcR3 is up-regulated in tumor tissues and is detectable in the sera of cancer patients, it is regarded as an immunosuppressor to down-regulate immune responses. To understand the function of DcR3 in vivo, we generated transgenic mice overexpressing DcR3 systemically. In comparison with HNT-TCR (HNT) transgenic mice, up-regulation of IL-4 and IL-10 and down-regulation of IFN-gamma, IL-12, and TNF-alpha were observed in the influenza hemagglutinin(126-138) peptide-stimulated splenocytes of HNT-DcR3 double-transgenic mice. When infected with Listeria monocytogenes, DcR3 transgenic mice show attenuated expression of IFN-gamma as well as increased susceptibility to infection. The Th2 cell-biased phenotype in DcR3 transgenic mice is attributed to decreased IL-2 secretion by T cells, resulting in the suppression of IL-2 dependent CD4(+) T cell proliferation. This suggests that DcR3 might help tumor growth by attenuating the Th1 response and suppressing cell-mediated immunity. |
