Abstract
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.
Publication types
-
Research Support, Non-U.S. Gov't
MeSH terms
-
Animals
-
Arenaviridae Infections / immunology
-
Blotting, Western
-
Cell Differentiation / immunology*
-
Cell Proliferation
-
Cytokines / biosynthesis
-
Lymphocyte Activation / immunology
-
Lymphocytic choriomeningitis virus / immunology
-
Mice
-
Mice, Inbred C57BL
-
Mice, Knockout
-
Nod Signaling Adaptor Proteins / immunology*
-
Nod Signaling Adaptor Proteins / metabolism
-
Receptor-Interacting Protein Serine-Threonine Kinase 2
-
Receptor-Interacting Protein Serine-Threonine Kinases / immunology*
-
Receptor-Interacting Protein Serine-Threonine Kinases / metabolism
-
T-Lymphocytes, Helper-Inducer / cytology
-
T-Lymphocytes, Helper-Inducer / immunology*
-
Toll-Like Receptors / immunology*
-
Toll-Like Receptors / metabolism
Substances
-
Cytokines
-
Nod Signaling Adaptor Proteins
-
Toll-Like Receptors
-
Receptor-Interacting Protein Serine-Threonine Kinase 2
-
Receptor-Interacting Protein Serine-Threonine Kinases
-
Ripk2 protein, mouse