Characterization of Signaling Pathways Activated by the Interleukin 1 (IL-1) Receptor Homologue T1/ST2

Brint, Elizabeth; Fitzgerald, Katherine A.; Smith, Philip; Coyle, Anthony J.; Gutierrez-Ramos, José-Carlos; Fallon, Padraic G.; O’Neill, Luke A. J.

doi:10.1074/jbc.m209685200

Cited by 75 publications

(60 citation statements)

References 49 publications

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“…We also show that central signaling pathways activated by IL-33 are comparable to IL-1. We detected NF-B activation by IL-33 and IL-1, which is in contrast to the data obtained in the chimeric model (27), but in accordance with transiently transfected HEK293 cells (1). This discrepancy may be because chimeric molecules were used, which may behave differently to the wild-type IL-33R␣-chain ligated with IL-33 (27).…”

Section: Discussioncontrasting

confidence: 55%

“…We did not generate a C-terminally truncated version of the IL-33R␣-chain in this study to prove stringently that in fact both TIR domains are essential for IL-33 signaling. However, similar studies (12,27) show that signaling is only possible when the TIR domain is present in ST2. Therefore, we must conclude that the TIR domains of the ␣-and ␤-chains are required for signal initiation.…”

Section: Discussionmentioning

confidence: 97%

“…Independently, chimeric receptor molecules of the then-orphan receptor ST2 were generated to investigate the signaling pathways activated by its cytoplasmic TIR domain. In D6/76 cells, IL-1RAcP served as a coreceptor for the ST2-chimera; however, no activation of NF-B was detectable (27).…”

Section: Discussionmentioning

confidence: 99%

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IL-1 receptor accessory protein is essential for IL-33-induced activation of T lymphocytes and mast cells

Ali

Huber

Kollewe³

et al. 2007

Proc. Natl. Acad. Sci. U.S.A.

302

275

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Section: Discussioncontrasting

confidence: 55%

Section: Discussionmentioning

confidence: 97%

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IL-1 receptor accessory protein is essential for IL-33-induced activation of T lymphocytes and mast cells

Ali

Huber

Kollewe³

et al. 2007

Proc. Natl. Acad. Sci. U.S.A.

302

275

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“…The P815 mastocytoma cell line was previously shown to express T1/ST2 [14]. We first examined whether IL-33 activates transcription factor pathways similar to those associated with intracellular IL-1 signaling.…”

Section: Il-33 Induces Il-6 Production By P815 Mastocytoma Cellsmentioning

confidence: 99%

Interleukin (IL)-33 induces the release of pro-inflammatory mediators by mast cells

Donzé²,

et al. 2007

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IL-33 (or IL-1F11) was recently identified as a ligand for the previously orphaned IL-1 family receptor T1/ST2. Previous studies have established that IL-33 and T1/ST2 exert key functions in Th2 responses. In this study, we demonstrate that IL-33 induces the production of pro-inflammatory mediators in mast cells. IL-33 dose and time-dependently stimulated IL-6 secretion by P815 mastocytoma cells and primary mouse bone marrow-derived mast cells (BMMC). This effect was dependent on T1/ST2 binding. In addition, IL-33 also induced IL-1b, TNF-a, MCP-1, and PGD2 production in BMMC. By RNase protection assay, we demonstrated that IL-33 increased IL-6 and IL-1b mRNA expression. These effects of IL-33 appeared to occur independently of mast cell degranulation, The results of this study show for the first time that IL-33, a novel member of the IL-1 family of cytokines, stimulates the production of pro-inflammatory mediators by mast cells in addition to its effect on T helper 2 responses. These findings open new perspectives for the treatment of inflammatory diseases by targeting IL-33.

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“…TLRs belong to a broader family of proteins, which include receptors for the proinflammatory cytokines IL-1 and IL-18 and the orphan receptor T1͞ST2 (11). All members of this superfamily signal inflammation in a very similar manner because of the presence of a conserved protein sequence in the cytosolic domain called the Toll͞IL-1 receptor domain, which activates common signaling pathways, most notably those leading to the activation of the transcription factor NF-B and stress-activated protein kinases (11).…”

mentioning

confidence: 99%

TLR2 is expressed on activated T cells as a costimulatory receptor

Komai-Koma

Jones

Ogg

et al. 2004

Proc. Natl. Acad. Sci. U.S.A.

430

455

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Toll is the founder of a group of pattern recognition receptors that play a critical role in the innate immunity in Drosophila. At least 10 distinct Toll-like receptors (TLRs), recognizing pathogen-associated molecular patterns, have now been identified in humans. Most investigations on TLRs have focused on cells of the innate system. We report here that naïve human T cells expressed high levels of cellsurface TLR2 after activation by anti-T cell receptor antibody and IFN-␣. Activated cells produced elevated levels of cytokines in response to the TLR2 ligand, bacterial lipopeptide. Furthermore, CD4 ؉ CD45RO ؉ memory T cells from peripheral blood constitutively expressed TLR2 and produced IFN-␥ in response to bacterial lipopeptide, which also markedly enhanced the proliferation and IFN-␥ production by CD45RO ؉ T cells in the presence of IL-2 or IL-15. Thus, TLR2 serves as a costimulatory receptor for antigen-specific T cell development and participates in the maintenance of T cell memory. This suggests that pathogens, via their pathogen-associated molecular patterns, may contribute directly to the perpetuation and activation of long-term T cell memory in both antigen-dependent and independent manner.

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Characterization of Signaling Pathways Activated by the Interleukin 1 (IL-1) Receptor Homologue T1/ST2

Cited by 75 publications

References 49 publications

IL-1 receptor accessory protein is essential for IL-33-induced activation of T lymphocytes and mast cells

IL-1 receptor accessory protein is essential for IL-33-induced activation of T lymphocytes and mast cells

Interleukin (IL)-33 induces the release of pro-inflammatory mediators by mast cells

TLR2 is expressed on activated T cells as a costimulatory receptor

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