First Author | Kim EM | Year | 2011 |
Journal | Mol Immunol | Volume | 48 |
Issue | 15-16 | Pages | 2189-97 |
PubMed ID | 21632113 | Mgi Jnum | J:177224 |
Mgi Id | MGI:5294511 | Doi | 10.1016/j.molimm.2011.05.002 |
Citation | Kim EM, et al. (2011) 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 NFkappaB into the nucleus. Mol Immunol 48(15-16):2189-97 |
abstractText | 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 IkappaBalpha have been shown to be actively involved in NFkappaB 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 NFkappaB. 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 (A(b)) 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 NFkappaB into the nucleus, which led to the polarization of naive CD4(+) T cells to T helper 2 (Th2) shift in vitro. Further analyses showed that SUMO-2 directly modified IkappaBalpha. These results indicate that the functional role of SUMO-2/3 in the regulation of NFkappaB activity was conserved during evolution. |