RIP2 contributes to Nod signaling but is not essential for T cell proliferation, T helper differentiation or TLR responses.

Håkan T L Hall, Margareta T Wilhelm, Samuel D Saibil, Tak W Mak, Richard A Flavell, Pamela S Ohashi

Campbell Family Institute for Breast Cancer Research, Ontario Cancer Institute, Department of Immunology, University of Toronto, Toronto, Canada.

European journal of immunology 2008 Jan

filter terms:

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.

Citation

Håkan T L Hall, Margareta T Wilhelm, Samuel D Saibil, Tak W Mak, Richard A Flavell, Pamela S Ohashi. RIP2 contributes to Nod signaling but is not essential for T cell proliferation, T helper differentiation or TLR responses. European journal of immunology. 2008 Jan;38(1):64-72