{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,12]],"date-time":"2026-02-12T15:33:55Z","timestamp":1770910435078,"version":"3.50.1"},"reference-count":30,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2007,12,12]],"date-time":"2007-12-12T00:00:00Z","timestamp":1197417600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Eur J Immunol"],"published-print":{"date-parts":[[2008,1]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Receptor\u2010interacting protein\u20042 (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\u2010binding oligomerization domain (Nod) signaling. Because initial reports remain controversial, we have further examined both innate and adaptive immune responses in RIP2\u2010deficient mice on the C57BL\/6 background. Despite the up\u2010regulation of RIP2 after T cell activation, we could not detect any defect in T cell proliferation or Th1\/Th2 responses in RIP2\u2010KO mice. Furthermore, we found that TLR responses in RIP2\u2010deficient macrophages were normal. However, our analysis showed that Nod signaling was impaired in macrophages from RIP2\u2010deficient mice. In conclusion, our data demonstrate a critical role for RIP2 in Nod signaling, while T cell proliferation, T\u2004helper differentiation and TLR responses were unaffected by the absence of RIP2.<\/jats:p>","DOI":"10.1002\/eji.200737393","type":"journal-article","created":{"date-parts":[[2007,12,17]],"date-time":"2007-12-17T23:16:55Z","timestamp":1197933415000},"page":"64-72","source":"Crossref","is-referenced-by-count":41,"title":["RIP2 contributes to Nod signaling but is not essential for T cell proliferation, T\u2004helper differentiation or TLR responses"],"prefix":"10.1002","volume":"38","author":[{"given":"H\u00e5kan\u2004T.\u2004L.","family":"Hall","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Margareta\u2004T.","family":"Wilhelm","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Samuel\u2004D.","family":"Saibil","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Tak\u2004W.","family":"Mak","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Richard\u2004A.","family":"Flavell","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Pamela\u2004S.","family":"Ohashi","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[2007,12,21]]},"reference":[{"key":"e_1_2_8_1_2","doi-asserted-by":"publisher","DOI":"10.1038\/sj.cdd.4401850"},{"key":"e_1_2_8_2_2","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.R500001200"},{"key":"e_1_2_8_3_2","doi-asserted-by":"publisher","DOI":"10.1038\/sj.cdd.4401890"},{"key":"e_1_2_8_4_2","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.273.20.12296"},{"key":"e_1_2_8_5_2","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.273.27.16968"},{"key":"e_1_2_8_6_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0960-9822(07)00352-1"},{"key":"e_1_2_8_7_2","doi-asserted-by":"publisher","DOI":"10.1093\/embo-reports\/kve155"},{"key":"e_1_2_8_8_2","doi-asserted-by":"publisher","DOI":"10.1038\/416194a"},{"key":"e_1_2_8_9_2","doi-asserted-by":"publisher","DOI":"10.1038\/416190a"},{"key":"e_1_2_8_10_2","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.C300460200"},{"key":"e_1_2_8_11_2","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M410114200"},{"key":"e_1_2_8_12_2","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.178.4.2380"},{"key":"e_1_2_8_13_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.immuni.2006.08.023"},{"key":"e_1_2_8_14_2","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.175.12.8051"},{"key":"e_1_2_8_15_2","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.178.6.3466"},{"key":"e_1_2_8_16_2","doi-asserted-by":"publisher","DOI":"10.1084\/jem.20061523"},{"key":"e_1_2_8_17_2","doi-asserted-by":"publisher","DOI":"10.1126\/science.1124256"},{"key":"e_1_2_8_18_2","doi-asserted-by":"crossref","first-page":"4302","DOI":"10.4049\/jimmunol.154.9.4302","article-title":"Fas ligand\u2010mediated cytotoxicity is directly responsible for apoptosis of normal CD4+ T cells responding to a bacterial superantigen.","volume":"154","author":"Ettinger R.","year":"1995","journal-title":"J. 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