Special aspects of interleukin-33 and the IL-33 receptor complex

Martin, Michael U.

doi:10.1016/j.smim.2013.10.006

Cited by 68 publications

(67 citation statements)

References 108 publications

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“…A member of the IL-1 family, IL-33 is expressed primarily by stromal cells, such as epithelial cells, endothelial cells, and fibroblasts, as well as by certain hematopoietic cells, including MC themselves (24)(25)(26). IL-33 is an "alarmin" released upon cell necrosis and also can be secreted by live cells after mechanical stretching and via other incompletely defined mechanisms (27,28). Its receptor ST2 (also called IL-1 receptor-related protein 1) is highly expressed by MC.…”

mentioning

confidence: 99%

IL-33/ST2 axis promotes mast cell survival via BCLXL

Wang

Kaieda

Ameri

et al. 2014

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

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Mast cells (MC) are potent innate immune cells that accumulate in chronically inflamed tissues. MC express the IL-33 receptor IL-1 receptor-related protein ST2 at high level, and this IL-1 family cytokine both activates MC directly and primes them to respond to other proinflammatory signals. Whether IL-33 and ST2 play a role in MC survival remains to be defined. In skin-derived human MC, we found that IL-33 attenuated MC apoptosis without altering proliferation, an effect mediated principally through the antiapoptotic molecule B-cell lymphoma-X large (BCLXL). Murine MC demonstrated a similar mechanism, dependent entirely on ST2. In line with these observations, St2−/− mice exhibited reduced numbers of tissue MC in inflamed arthritic joints, in helminthinfected intestine, and in normal peritoneum. Together, these data reveal a cell-intrinsic role for the IL-33/ST2 axis in the regulation of apoptosis in MC, identifying thereby a previously unappreciated pathway supporting expansion of the MC population with inflammation.arthritis | helminth infection M ast cells (MC) are tissue-resident effector cells that contribute both to innate and adaptive immunity (1). MC help defend against bacterial and helminthic infection (2, 3) and play a role in tissue remodeling (4, 5). MC can also contribute to a variety of allergic and nonallergic inflammatory diseases, such as anaphylaxis, atopic dermatitis, asthma, inflammatory arthritis, psoriasis, and multiple sclerosis (6, 7). Under many of these conditions, the number of MC in affected tissues increases by tenfold or more, amplifying the contribution of MC-derived mediators to ongoing inflammation (6-8). Regulation of the MC population is poorly understood, and therapeutic intervention to limit MC accumulation potentially could attenuate injury associated with inflammatory diseases (9, 10).The survival of mature MC in tissues depends on signals from neighboring cells (11,12). The single most important mediator in this process is stem cell factor (SCF), a master regulator of MC proliferation, differentiation, survival, and activation. Mice with genetic mutations affecting SCF or its receptor Kit have few or no MC in healthy or inflamed tissues, whereas activating mutations of Kit give rise to pathologic mastocytosis (13-15). IL-3 is another well-recognized MC growth factor (16). SCF/Kit and IL-3 interface with several antiapoptotic pathways, up-regulating the antiapoptotic protein B-cell lymphoma-2 (BCL-2) and downregulating the proapoptotic protein Bim (14,(17)(18)(19). Aside from SCF/Kit and IL-3, other cytokines have been reported to support MC survival, but their effects appear to be restricted to specific MC subtypes. IL-4 promotes survival of intestinal MC via both BCL-2 and B-cell lymphoma-X large (BCLXL) but may suppress survival in human cord blood MC as well as murine bone marrowderived MC (BMMC) (20-23). IL-10 can either promote or impair survival depending on the type of MC studied (21,22).Recently, substantial attention has focused on the role of IL-33 in MC biolog...

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confidence: 99%

IL-33/ST2 axis promotes mast cell survival via BCLXL

Wang

Kaieda

Ameri

et al. 2014

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

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“…IL-33 is a member of the IL-1 cytokine family, and is constitutively expressed in epithelial cells, endothelial cells and fibroblasts [3]. IL-33 consists of two domains: a non-classical homeodomain-like helix-turn-helix DNA-binding domain, which consists of a chromatin-binding motif (CBM) and a nuclear localization sequence (NLS), and an IL-1-like domain [4] (Fig. 25.1a).…”

Section: Introductionmentioning

confidence: 99%

“…IL-33 signals through the IL-33 receptor (IL-33R), which consists of heterodimers of ST2 and IL-1 receptor accessory protein (IL-1RAcP) [5,6] (Fig. 25.2 [4][5][6] cytoplasmic region of ST2. The MyD88 and TRAF6 complex activates NF-κB-and MAP kinase-mediated signaling pathways [5,6].…”

Section: Introductionmentioning

confidence: 99%

Possible Roles of IL-33 in Periodontal Diseases: Porphyromonas gingivalis Induced IL-33 in Human Gingival Epithelial Cells

Tada

Shimauchi

Takada

et al. 2015

Interface Oral Health Science 2014

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In the oral mucosa, epithelial cells work not only as a physical barrier to pathogens, but also play a pivotal role in initiating immune responses to microbes. Interleukin (IL)-33, a member of the IL-1 family, is constitutively expressed in epithelial cells and amplifies Th2-type inflammatory immune responses. We found that IL-33 was detected in the inflamed gingival epithelium from chronic periodontitis patients, and periodontopathic Porphyromonas gingivalis strongly increased expressions of IL-33 mRNA and molecules in human gingival epithelial cells. In contrast, fimbriae, a lipopeptide and lipopolysaccharide derived from P. gingivalis were not active in this respect. Protease inhibitors specific for gingipains efficiently inhibited the induction of IL-33 mRNA by stimulation with P. gingivalis. Furthermore, P. gingivalis KDP136, a gingipains-null mutant, did not increase IL-33 mRNA expression. We also demonstrated that P. gingivalis upregulated IL-33 mRNA expression through protease-activated receptor-2, phospholipase C, mitogen-activated protein kinase p38 and NF-κB. IL-33 is suggested to negatively regulate antimicrobial peptide LL-37, resulting in attenuation of innate immune responses of gingival epithelial cells in chronic periodontitis. Possible roles of IL-33 in inflammation in the oral mucosa are discussed.

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“…IL-33 is released from damaged cells by necrosis, and acts as an alarmin released from necrotic cells (12). Moreover, IL-33 is also produced by living cells after mechanical stress.…”

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confidence: 99%

“…In contrast, abundant evidence suggests that IL-33 is also involved in the development of chronic inflammatory diseases such as arthritis (25). IL-33 is induced in response to such fungal allergens as Alternaria infection, ragweed pollen, and proinflammatory cytokines, and it induces the production of Th2 cytokines by group 2 innate lymphoid cells, for the initiation of allergic inflammation in response to pathogens (12,13,21,22). USA).…”

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confidence: 99%

Increases in IL-33 production by fimbriae and lipopeptide from Porphyromonas gingivalis in mouse bone marrow-derived dendritic cells via Toll-like receptor 2

et al. 2017

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Interleukin-33 (IL-33) is an IL-1 cytokine family member that is involved in the development of chronic inflammatory diseases and the initiation of allergic inflammation in response to pathogens. Porphyromonas gingivalis is a primary pathogen that is involved in chronic periodontitis and its bacterial components induce inflammatory responses. Dendritic cells (DCs) recognize pathogenassociated molecular patterns by expression of pattern-recognition receptors, such as Toll-like receptors (TLRs). DCs play an essential role in resistance to infection and maintenance of mucosal immune system. In this study, we investigated whether P. gingivalis increases the expression of IL-33 in mouse bone marrow-derived DCs (BMDCs). BMDCs exhibited an increased expression of IL-33 mRNA upon stimulation with P. gingivalis whole cells. Furthermore, fimbriae and lipopeptide derived from P. gingivalis exhibited higher IL-33 mRNA expression than P. gingivalis whole cells. In contrast, lipopolysaccharide derived from P. gingivalis did not induce IL-33 mRNA expression in BMDCs. The IL-33 mRNA expression after stimulation with fimbriae or lipopeptide was up-regulated in BMDCs from wild-type mice but not from TLR2-deficient (TLR2

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Special aspects of interleukin-33 and the IL-33 receptor complex

Cited by 68 publications

References 108 publications

IL-33/ST2 axis promotes mast cell survival via BCLXL

IL-33/ST2 axis promotes mast cell survival via BCLXL

Possible Roles of IL-33 in Periodontal Diseases: Porphyromonas gingivalis Induced IL-33 in Human Gingival Epithelial Cells

<b>Increases in IL-33 production by fimbriae and lipopeptide from </b><i><b>Porphyromonas gingivalis</b></i><b> in mouse bone marrow-derived dendritic cells via Toll-like receptor </b><b>2 </b>

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