Interleukin (IL)-22 and IL-17 are coexpressed by Th17 cells and cooperatively enhance expression of antimicrobial peptides

Liang, Spencer; Tan, Xiang-Yang; Luxenberg, Deborah; Karim, Riyez; Dunussi‐Joannopoulos, Kyriaki; Collins, Mary; Fouser, Lynette A.

doi:10.1084/jem.20061308

Cited by 2,044 publications

(1,932 citation statements)

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“…More recently, it has been argued that Th17 cells are also major producers of IL-22 (12,42). The current view of mouse Th17 development is that TGF␤1 and IL-6 are the key cytokines that initiate the differentiation process and that IL-23 plays an essential role in the expansion and maintenance of this lineage.…”

Section: Discussionmentioning

confidence: 99%

“…IL-22 is a member of the IL-10 family, and its gene is located on chromosome 12q15 between the IFN␥ and IL-26 loci (40,41). Recently, IL-22 has been reported to be produced by murine Th17 cells in vitro and in vivo (12,42). We sought to determine whether the expression of IL-22 in human CD4ϩ T cells was regulated in the same manner as that of IL-17A and IL-17F.…”

Section: Il-17 Regulation In Human T Cells 2941mentioning

confidence: 99%

“…Similarly, anti-p40 antibody is efficacious in the treatment of Crohn's disease (7). Although these effects were initially misattributed to interference with the actions of IL-12, using specific deletion of IL-23 (p19 Ϫ/Ϫ mice), it is now recognized that IL-23 (and not IL-12) is the culprit, at least in many of the animal models (8)(9)(10)(11)(12)(13).…”

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confidence: 99%

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Distinct regulation of interleukin‐17 in human T helper lymphocytes

Chen¹,

Tato²,

Muul³

et al. 2007

Arthritis & Rheumatism

317

281

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Section: Discussionmentioning

confidence: 99%

Section: Il-17 Regulation In Human T Cells 2941mentioning

confidence: 99%

See 1 more Smart Citation

Distinct regulation of interleukin‐17 in human T helper lymphocytes

Chen¹,

Tato²,

Muul³

et al. 2007

Arthritis & Rheumatism

317

281

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“…IL-22 was first reported to be associated with Th1 cells but was subsequently shown to be secreted by Th17 cells, gdT cells, NKT cells, NK cells, CD11c 1 myeloid cells and lymphoid tissue inducer-like cells [16][17][18][19]. The in vitro differentiation of Th17 cells produces a population of cells with a single expression of IL-17 and IL-22 and the coexpression of IL-17 and IL-22 [16]. Although both IL-6 and TGF-b are necessary for Th17 cell differentiation, IL-6 or IL-23 induces IL-22 production, whereas TGF-b inhibits IL-22 production [4].…”

Section: Introductionmentioning

confidence: 99%

Regulation of the development of acute hepatitis by IL‐23 through IL‐22 and IL‐17 production

Morishima

Mizoguchi

et al. 2011

Eur J Immunol

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IL-23 plays a critical role in the expansion of highly proinflammatory Th17 cells secreting . Recently, we demonstrated that Notch signaling drives IL-22 secretion through the aryl hydrocarbon receptor (AHR) and plays a protective role in Con A-induced hepatitis. In this study, we investigated the role of IL-23 in hepatitis using IL-23p19-and IL-17-deficient mice. In WT mice, the injection of Con A induced the upregulation of various cytokines, which included IL-23, IL-22, IL-17, IFN-c and TNF-a. In IL-23p19-deficient mice, exacerbated hepatitis was observed and serum IL-22 and IL-17 levels were greatly reduced, whereas in IL-17-deficient mice, ameliorated hepatitis was observed. The injection of exogenous IL-22 protected p19-deficient mice from hepatitis, whereas the injection of exogenous IL-23 significantly increased the serum levels of not only IL-22 but also IL-17, and less effectively protected against hepatitis in IL-17-dependent and -independent manners. Finally, it was revealed that STAT3, STAT4 and Notch contributed to the production of both the cytokines, and that the AHR was important only for IL-22 production in response to Con A and IL-23 in liver mononuclear cells. These results suggest that IL-23 plays a protective role in hepatitis through IL-22 production and also a pathological role via IL-17-dependent and -independent mechanisms.Key words: Hepatitis . IL-17 . IL-22 . IL-23Supporting Information available online Introduction IL-23 is a heterodimeric cytokine which belongs to the IL-6/IL-12 family and plays a key role in autoimmune and inflammatory disorders [1]. IL-23 acts on memory-type cells [2] and induces the production of . Moreover, IL-23 is an essential factor in the survival and expansion of Th17 cells [5], which produce cytokines including IL-17, IL-17F, . p19-deficient mice are highly resistant to the development of experimental allergic encephalomyelitis (EAE) [7], and it has been shown that the IL-23-dependent production of IL-17, but not , is important for the pathogenesis of autoimmune 2828diseases such as EAE [9]. Recent studies have also revealed that the IL-23-dependent production of IL-22, but not IL-17, plays a critical role in protection against subsequent infection. In infection with an attenuated strain of Salmonella enterica serovar Enteritidis, p19-deficient mice showed reduced survival and exacerbated liver necrosis only in the absence of IL-12 in an IL-17-independent manner [10]. In peroral infection with Toxoplasma gondii, which leads to the development of small intestine inflammation, the IL-23-dependent upregulation of IL-22 is essential for the development of ileitis; on the other hand, IL-17 is downregulated and dispensable [11].IL-22 is a member of the IL-10 cytokine family and plays important roles in inflammation, immune surveillance and tissue homeostasis [12][13][14][15] [10,25,26].Recently, we demonstrated that Notch, which is an evolutionally conserved molecule that controls cell fate decision in a variety of cells [27,28], drives IL-22 secretion by stimu...

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“…Expression analysis has revealed that IL-22 was significantly induced in lymphoid tissues including spleen and intestine. This is not surprising since IL-22 is known to be the key cytokine in mediating immune defense against extracellular bacterial pathogens (Liang et al 2006). The fact that poly(I:C) also induced IL-22 and IL-26 expression in spleen suggests that they may have some roles in host antiviral defense.…”

Section: Discussionmentioning

confidence: 97%

Comparative study and expression analysis of the interferon gamma gene locus cytokines in Xenopus tropicalis

Nie

2008

Immunogenetics

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Using bioinformatics approach, the genome locus containing interleukin (IL)-22, IL-26, and interferon gamma (IFN-γ) genes has been identified in the amphibian, Xenopus tropicalis. Like that in other vertebrates such as fish, birds, and mammals, the Xenopus IL-22, IL-26, and IFN-γ are clustered in the same chromosome and the adjacent genes are conserved. The genomic structures of the Xenopus IL-22, IL-26, and IFN-γ gene were identical to that of their mammalian counterparts. The Xenopus IL-22 and IL-26 genes contained five exons and four introns while the Xenopus IFN-γ gene consisted of four exons and three introns. The Xenopus IL-22, IL-26, and IFN-γ share 14.1-41.6%, 14.6-31.2%, and 23.7-36.5% identity to their counterparts in other species, respectively. Reversetranscription polymerase chain reaction (PCR) and realtime quantitative PCR analyses revealed that the expression of IL-22, IL-26, and IFN-γ genes was significantly upregulated after simulation with bacterial polyliposaccharide and/or synthetic double-stranded poly(I:C), suggesting these cytokines like those in other vertebrates play an important role in regulating immune response in Xenopus.

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Interleukin (IL)-22 and IL-17 are coexpressed by Th17 cells and cooperatively enhance expression of antimicrobial peptides

Cited by 2,044 publications

References 19 publications

Distinct regulation of interleukin‐17 in human T helper lymphocytes

Distinct regulation of interleukin‐17 in human T helper lymphocytes

Regulation of the development of acute hepatitis by IL‐23 through IL‐22 and IL‐17 production

Comparative study and expression analysis of the interferon gamma gene locus cytokines in Xenopus tropicalis

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