The mouse small ubiquitin-like modifier-2 (SUMO-2) inhibits interleukin-12 (IL-12) production in mature dendritic cells by blocking the translocation of the p65 subunit of NFκB into the nucleus

Eun Mi Kim, Han Hyoung Lee, Sang Hoon Kim, Young Ok Son, Suk Jun Lee, Jihye Han, Joonbeom Bae, Sang Joon Kim, Chung Gyu Park, Yongsoo Park, Kwang Woo Hwang, Taehoon Chun

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16 Citations (Scopus)


Post-translational modification by small ubiquitin-like modifier (SUMO) is involved in several significant cellular events. In particular, SUMO-1 and SUMO-4 modifications of IκBα have been shown to be actively involved in NFκB regulation. However, among the SUMO family, the specific function of SUMO-2/3 remains relatively unknown. In addition, it is not clear whether SUMO-2/3 follows the same functional role as SUMO-1 and SUMO-4 during the activation of NFκB. In this study, we examined the influence of mouse SUMO-2 during the maturation of dendritic cells (DCs). Our results showed that the ectopic expression of SUMO-2 does not affect the cell surface expression of MHC class II molecule (Ab) and co-stimulatory molecules (CD80 and CD86), and the efficiency of antigen uptake. However, the ectopic expression of mouse SUMO-2 inhibited IL-12 secretion by blocking the translocation of the p65 subunit of NFκB into the nucleus, which led to the polarization of naïve CD4+ T cells to T helper 2 (Th2) shift in vitro. Further analyses showed that SUMO-2 directly modified IκBα. These results indicate that the functional role of SUMO-2/3 in the regulation of NFκB activity was conserved during evolution.

Original languageEnglish
Pages (from-to)2189-2197
Number of pages9
JournalMolecular Immunology
Issue number15-16
Publication statusPublished - 2011 Sep 1



  • Dendritic cells
  • IL-12
  • NFκB
  • Post-translational modification
  • Sumoylation

ASJC Scopus subject areas

  • Immunology
  • Molecular Biology

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