T-helper 17 and Interleukin-17–Producing Lymphoid Tissue Inducer-Like Cells Make Different Contributions to Colitis in Mice

Ono, Yūichi; Kanai, Takanori; Sujino, Tomohisa; Nemoto, Yasuhiro; Kanai, Yasumasa; Mikami, Yohei; Hayashi, Akira; Matsumoto, Atsuhiro; Takaishi, Hiromasa; Ogata, Haruhiko; Matsuoka, Katsuyoshi; Hisamatsu, Tadakazu; Watanabe, Mamoru; Hibi, Toshifumi

doi:10.1053/j.gastro.2012.07.108

Cited by 34 publications

(27 citation statements)

References 23 publications

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“…In addition to CD4 ϩ T cells, other cell populations have recently been shown to produce IL-17 by either direct or indirect stimulation by microbes or their stimuli during infection. CD8 ϩ cytotoxic T cells, ␥␦ T cells, NK cells, NKT cells, and LTi cells are among the populations that are significant producers of IL-17A upon stimulation (16,27,29,54,56,58,68,75). To confirm our in vitro findings with CD4 ϩ T cells and further determine which of the above populations contribute to IL-17A production in vivo during S. Typhimurium infection, we employed a multicolor flow cytometry approach.…”

Section: Characterization Of the Curli Mutantmentioning

confidence: 74%

Microbial Amyloids Induce Interleukin 17A (IL-17A) and IL-22 Responses via Toll-Like Receptor 2 Activation in the Intestinal Mucosa

et al. 2012

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The Toll-like receptor 2 (TLR2)/TLR1 receptor complex responds to amyloid fibrils, a common component of biofilm material produced by members of the phyla Firmicutes, Bacteroidetes, and Proteobacteria. To determine whether this TLR2/TLR1 ligand stimulates inflammatory responses when bacteria enter intestinal tissue, we investigated whether expression of curli amyloid fibrils by the invasive enteric pathogen Salmonella enterica serotype Typhimurium contributes to T helper 1 and T helper 17 responses by measuring cytokine production in the mouse colitis model. A csgBA mutant, deficient in curli production, elicited decreased expression of interleukin 17A (IL-17A) and IL-22 in the cecal mucosa compared to the S. Typhimurium wild type. In TLR2-deficient mice, IL-17A and IL-22 expression was blunted during S. Typhimurium infection, suggesting that activation of the TLR2 signaling pathway contributes to the expression of these cytokines. T cells incubated with supernatants from bone marrow-derived dendritic cells (BMDCs) treated with curli fibrils released IL-17A in a TLR2-dependent manner in vitro. Lower levels of IL-6 and IL-23 production were detected in the supernatants of the TLR2-deficient BMDCs treated with curli fibrils. Consistent with this, three distinct T-cell populations-CD4؉ T helper cells, cytotoxic CD8 ؉ T cells, and ␥␦ T cells-produced IL-17A in response to curli fibrils in the intestinal mucosa during S. Typhimurium infection. Notably, decreased IL-6 expression by the dendritic cells and decreased IL-23 expression by the dendritic cells and macrophages were observed in the cecal mucosa of mice infected with the curli mutant. We conclude that TLR2 recognition of bacterial amyloid fibrils in the intestinal mucosa represents a novel mechanism of immunoregulation, which contributes to the generation of inflammatory responses, including production of IL-17A and IL-22, in response to bacterial entry into the intestinal mucosa.

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Section: Characterization Of the Curli Mutantmentioning

confidence: 74%

Microbial Amyloids Induce Interleukin 17A (IL-17A) and IL-22 Responses via Toll-Like Receptor 2 Activation in the Intestinal Mucosa

et al. 2012

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“…Exposure of PBMC-derived Th17 cells to UCB resulted in an increase in the frequency of IL-10-producing cells ( Figure 2A); this increase was mirrored by increases in the IL-10 mean fluorescence intensity (MFI) ( Figure 2B) and mRNA levels ( Figure 2C). UCB, however, did not alter other aspects of the Th17 cell phenotype, as reflected by levels of IL-17, RAR-related orphan receptor C (RORC), IL-23 receptor (IL-23R), and CCR6 expression ( Figure 2D), but rather diminished the expression of IL-22 and IL-1β, cytokines typically expressed by pathogenic Th17 cells ( Figure 2E) (33,34). UCB markedly abrogated Th17 cell proliferation ( Figure 2F) without, however, increasing the cell apoptotic rate, as determined by the frequency of annexin V + cells ( Figure 2G).…”

Section: Resultsmentioning

confidence: 98%

Bilirubin suppresses Th17 immunity in colitis by upregulating CD39

et al. 2017

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“…Th17 cells were initially reported to have proinflammatory properties and therefore to play a major role in autoimmune and chronic inflammatory diseases (Langrish et al, 2005;Harrington et al, 2005;Park et al, 2005). However, later it was found that Th17 cells can also produce IL-10 and display potent anti-inflammatory, regulatory properties (Zielinski et al, 2012;Ono et al, 2012;Esplugues et al, 2011;McGeachy et al, 2007). These regulatory Th17 cells have been called rTh17 Li and Flavell, 2008).…”

Section: Regulatory Th17 Cellsmentioning

confidence: 99%