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Blood, 4 June 2009, Vol. 113, No. 23, pp. 5891-5895. Prepublished online as a Blood First Edition Paper on April 2, 2009; DOI 10.1182/blood-2008-08-175489. This Article Full Text Full Text (PDF) Supplemental Figure All Versions of this Article: blood-2008-08-175489v1 113/23/5891    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via CrossRef Google Scholar Articles by Srokowski, C. C. Articles by Schild, H. PubMed PubMed Citation Articles by Srokowski, C. C. Articles by Schild, H. Related Collections Immunobiology Brief Reports Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  IMMUNOBIOLOGY Brief report Naturally occurring short splice variant of CYLD positively regulates dendritic cell function Cathy Cecilia Srokowski1,*, Joumana Masri2,*, Nadine Hövelmeyer2, Anna Katharina Krembel1, Christine Tertilt1, Dennis Strand2, Karsten Mahnke3, Ramin Massoumi4, Ari Waisman2,, and Hansjörg Schild1, 1 Institute for Immunology, and 2 First Department of Internal Medicine, Johannes Gutenberg University, Mainz, Germany; 3 Department of Dermatology, University of Heidelberg, Heidelberg, Germany; and 4 Department of Laboratory Medicine, Clinical Research Center, Lund University, Malmo, Sweden Deubiquitination of NF-B members by CYLD is crucial in controlling the magnitude and nature of cell activation. The role of the naturally occurring CYLD splice variant in dendritic cell (DC) function was analyzed using CYLDex7/8 mice, which lack the full-length CYLD (flCYLD) transcript and overexpress the short splice variant (sCYLD). Bone marrow–derived DCs from CYLDex7/8 mice display a hyperactive phenotype in vitro and in vivo and have a defect in establishing tolerance with the use of DEC-205–mediated antigen targeting to resting DCs. The combination of sCYLD overexpression and lack of flCYLD in CYLDex7/8 DCs leads to enhanced NF-B activity accompanied by an increased nuclear translocation of the IB molecule Bcl-3, along with nuclear p50 and p65. This suggests that, in contrast to flCYLD, sCYLD is a positive regulator of NF-B activity, and its overexpression induces a hyperactive phenotype in DCs. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this?

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