| First Author | Hall HT | Year | 2008 |
| Journal | Eur J Immunol | Volume | 38 |
| Issue | 1 | Pages | 64-72 |
| PubMed ID | 18085666 | Mgi Jnum | J:130818 |
| Mgi Id | MGI:3772393 | Doi | 10.1002/eji.200737393 |
| Citation | Hall HT, et al. (2008) RIP2 contributes to Nod signaling but is not essential for T cell proliferation, T helper differentiation or TLR responses. Eur J Immunol 38(1):64-72 |
| abstractText | Receptor-interacting protein 2 (RIP2), also known as CARDIAK and RICK, has been reported to play a role in both adaptive T cell responses and innate immunity as a mediator in TLR signaling and nucleotide-binding oligomerization domain (Nod) signaling. Because initial reports remain controversial, we have further examined both innate and adaptive immune responses in RIP2-deficient mice on the C57BL/6 background. Despite the up-regulation of RIP2 after T cell activation, we could not detect any defect in T cell proliferation or Th1/Th2 responses in RIP2-KO mice. Furthermore, we found that TLR responses in RIP2-deficient macrophages were normal. However, our analysis showed that Nod signaling was impaired in macrophages from RIP2-deficient mice. In conclusion, our data demonstrate a critical role for RIP2 in Nod signaling, while T cell proliferation, T helper differentiation and TLR responses were unaffected by the absence of RIP2. |
