Document Detail


IL-32{gamma} Induces the Maturation of Dendritic Cells with Th1- and Th17-Polarizing Ability through Enhanced IL-12 and IL-6 Production.
MedLine Citation:
PMID:  21551364     Owner:  NLM     Status:  Publisher    
Abstract/OtherAbstract:
IL-32, a newly described multifunctional cytokine, has been associated with a variety of inflammatory diseases, including rheumatoid arthritis, vasculitis, and Crohn's disease. In this study, we investigated the immunomodulatory effects of IL-32γ on bone marrow-derived dendritic cell (DC)-driven Th responses and analyzed the underlying signaling events. IL-32γ-treated DCs exhibited upregulated expression of cell-surface molecules and proinflammatory cytokines associated with DC maturation and activation. In particular, IL-32γ treatment significantly increased production of IL-12 and IL-6 in DCs, which are known as Th1- and Th17-polarizing cytokines, respectively. This increased production was inhibited by the addition of specific inhibitors of the activities of phospholipase C (PLC), JNK, and NF-κB. IL-32γ treatment increased the phosphorylation of JNK and the degradation of both IκBα and IκBβ in DCs, as well as NF-κB binding activity to the κB site. The PLC inhibitor suppressed NF-κB DNA binding activity and JNK phosphorylation increased by IL-32γ treatment, thereby indicating that IL-32γ induced IL-12 and IL-6 production in DCs via a PLC/JNK/NF-κB signaling pathway. Importantly, IL-32γ-stimulated DCs significantly induced both Th1 and Th17 responses when cocultured with CD4(+) T cells. The addition of a neutralizing anti-IL-12 mAb abolished the secretion of IFN-γ in a dose-dependent manner; additionally, the blockage of IL-1β and IL-6, but not of IL-21 or IL-23p19, profoundly inhibited IL-32γ-induced IL-17 production. These results demonstrated that IL-32γ could effectively induce the maturation and activation of immature DCs, leading to enhanced Th1 and Th17 responses as the result of increased IL-12 and IL-6 production in DCs.
Authors:
Mi Young Jung; Mi Hye Son; Soo Hyun Kim; Daeho Cho; Tae Sung Kim
Related Documents :
11742404 - C-myc regulates mammalian body size by controlling cell number but not cell size.
21357534 - Cutting edge: primary innate immune cells respond efficiently to polymeric peptidoglyca...
10919674 - E1a overcomes the apoptosis block in bcr-abl+ leukemia cells and renders cells suscepti...
21116974 - Method for analysis of nanoparticle effects on cellular chemotaxis.
16647244 - Immunity and emotions: lipopolysaccharide increases defensive behaviours and potentiate...
18615114 - Patients with chronic mucocutaneous candidiasis exhibit reduced production of th17-asso...
Publication Detail:
Type:  JOURNAL ARTICLE     Date:  2011-5-6
Journal Detail:
Title:  Journal of immunology (Baltimore, Md. : 1950)     Volume:  -     ISSN:  1550-6606     ISO Abbreviation:  -     Publication Date:  2011 May 
Date Detail:
Created Date:  2011-5-9     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  2985117R     Medline TA:  J Immunol     Country:  -    
Other Details:
Languages:  ENG     Pagination:  -     Citation Subset:  -    
Affiliation:
School of Life Sciences and Biotechnology, Korea University, Seoul 136-701, Republic of Korea;
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


Previous Document:  HIV-1 Reduces A{beta}-Degrading Enzymatic Activities in Primary Human Mononuclear Phagocytes.
Next Document:  Tumor-Infiltrating Programmed Death Receptor-1+ Dendritic Cells Mediate Immune Suppression in Ovaria...