Journal articles: 'Il-33 vih'

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S, Traoré. "Survie des personnes vivant avec le VIH et le Sida suivies dans les 17 sites de traitement antirétroviral au Mali." Mali Santé Publique 10, no. 02 (April 20, 2021): 44–49. http://dx.doi.org/10.53318/msp.v10i02.1796.

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Introduction : Au Mali, malgré de nombreuses campagnes de prévention et de l'efficacité de la thérapie antirétrovirale, les cas de décès liés au VIH touchent beaucoup plus les couches productives. Pour mieux élucider ce constat nous avons étudié la survie des Personnes Vivant avec le VIH suivies pendant 5 ans au Mali. Matériel et méthodes : Il s'agissait d'une étude de cohorte, incluant 39619 personnes vivant avec le VIH suivis pendant 5 ans sur les 17 sites d'ESOPE du Mali. Les données collectées concernent celles des années 1999 à 2014, elles ont été analysées par le logiciel STATA version 12. Résultats : Environ 13% des patients étaient décédés à la 5ème année. Le taux brut de mortalité était de 10,22 personnes année. A l'analyse uni variée, les femmes avaient un risque de décès significativement plus faible (33%) que les hommes (HR=0,67, IC95% = [0,62- 0,72]). Le risque ratio de décès des patients sous le traitement Antirétroviral était plus faible (43%) que ceux non-initiés aux ARV (HR=0,57, IC95% = [0,53-0,62]). Aussi bien à l'analyse uni-variée qu'à l'analyse multi-variée, le risque de décès des patients vus aux stades cliniques 3 et 4 de l'OMS à l'inclusion était significativement plus élevé comparé à ceux vus au stade 1. Conclusion : Nos résultats ont montré que la proportion de survie était de 87%. Le stade clinique de l'OMS, le sexe, le traitement antirétroviral étaient des facteurs de risque associés aux décès des patients. Mot clés : Survie, Personnes vivant avec le VIH, 1999 à 2014.

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Keita, BB, and Et Al. "Facteurs associés au décès des personnes infectées par le virus de l’immunodéficience humaine sous traitement antirétroviral au Centre Walé de Ségou, Mali." Revue Malienne d'Infectiologie et de Microbiologie 18, no. 2 (January 8, 2024): 38–49. http://dx.doi.org/10.53597/remim.v18i2.2733.

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Introduction : Bien que le rôle des facteurs cliniques/biologiques associés à la mortalité ait déjà été exploré chez les patients séropositifs. Cependant, peu d'attention a été accordée jusqu'à présent à l'impact potentiel de l'absence de soutien psychosocial sur la mortalité chez les PV VIH. L'objectif de ce travail était d'étudier non seulement les facteurs clinico-biologiques mais aussi l'impact du manque de soutien psychosocial sur la mortalité des patients atteints du VIH. Méthode et Matériels : Il s’agissait d’une étude de cohorte. La durée de suivi était de 5 ans (2017 à 2021). La collecte a été effectuée de façon rétrospective à travers les dossiers des 292 patients inclus sur un total de 320 patients. Les analyses statistiques ont été réalisées en utilisant le logiciel R version 4.2.2. Résultats : La prévalence de décès était de 33% de 2017 à 2021. Le taux brut de mortalité était de 24,42 pour 100 personnes année. La durée médiane de suivi était de 9 mois avec IQR : [4 ;26], le sexe ratio H/F était de 0,9. Après une analyse multivariée de Cox régressif , les facteurs significativement associés au décès étaient les stades 3 et 4 de l’OMS (HR=3, IC95%= [1,7-7,6], et (HR=14, IC95%=[6,9-32]), l’anémie (HR=2, IC95%= [1,1-3,8]), l’absence des activités associatives (HR=1.7, IC95%= [1-2.7]), le non-partage de son statut sérologique avec le conjoint(e) (HR=2, IC95%= [1,4-3,7]), vivre en zone rurale (HR= 2 ; IC95% = [2,2-3]) et les hommes ayant des rapports sexuels avec d’autres hommes (HR=1,8 ; IC95%= [1.17-2.9]). Conclusion : Le soutien psychosocial a un fort pouvoir de rétention, car il motive les personnes séropositives à accepter leur statut, avec des effets sur les résultats cliniques et biologiques. Il est donc utile d'explorer les facteurs qui conduisent à l'arrêt précoce du traitement ARV

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Abdourahimi, D., D. Yehadji, E. Briskin, E. M. Khine, C. Arias, K. S. André, F. K. Mukebela, et al. "Facteurs associés à la létalité chez les patients hospitalisés pour le VIH avancé." Public Health Action 13, no. 2 (August 1, 2023): 19–24. http://dx.doi.org/10.5588/pha.23.0009.

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CONTEXTE : Une unité soutenue par Médecins Sans Frontières (MSF) qui prend en charge les patients avec un VIH avancé à l’Hôpital National de Donka, Conakry, Guinée.OBJECTIF : Déterminer les facteurs liés à la survenue du décès chez les patients hospitalisés dans l’unité entre 2017 et 2021.SCHÉMA : Ceci est une analyse rétrospective de données de routine des patients hospitalisés pour le VIH avancé.RÉSULTATS : Au total, 3,718 patients étaient inclus, d’âge médian de 40 ans (IQR 33–51), dont 2,241 (60,3%) femmes. Le taux de moyen de décès était de 33,6% (n = 1,240). Il était passé de 40% en 2017 à 29% en 2021, sans être statistiquement significatif. La période la plus à risque de décès était les 25 premiers jours d’hospitalisation. Chez ces patients décédés, la TB (43,8%) et la toxoplasmose (11,4%) étaient les diagnostics les plus fréquents. Après analyse multivariée par régression de Cox, les facteurs associés au décès étaient un âge compris entre 25–49 ans (hazard ratio ajusté [HRa] 1,60 ; P = 0,002) ou 50 ans (HRa 1,80 ; P < 0,001), la présence de signes respiratoires (HRa 1,23 ; P = 0,001) ou abdominaux (HRa 1,26 ; P < 0,001) et une réadmission (HRa 0,54 ; P < 0,001).CONCLUSION : Les patients âgés de 25–49 ans, ou plus, ou présentant des signes respiratoires ou abdominaux requièrent une surveillance accrue car ils sont les plus à risque de décéder de la maladie, surtout pendant les 25 premiers jours d’hospitalisation.

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Beye, SA, and Et Al. "Prévalence des infections nosocomiales au Centre Hospitalier Universitaire du Point G de Bamako, Mali." Revue Malienne d'Infectiologie et de Microbiologie 19, no. 1 (March 13, 2024): 45–49. http://dx.doi.org/10.53597/remim.v19i1.2794.

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Objectifs de cette étude était de déterminer la prévalence hospitalière des infections nosocomiales. Patients et méthodes : Il s’agissait d’une étude prospective transversale descriptive sur une période de six (6) semaines. Résultats : 463 patients ont séjourné pendant au moins 48 heures. Parmi eux, 57 patients inclus soit une prévalence de 12,3%. L’âge moyen était de 45,4 ± 20,8 ans. La durée moyenne du séjour était de 21,7 ± 12,7 jours. Les patients provenaient de la réanimation (17,5%), la médecine interne et la neurologie dans 15,8% chacune. L’immunodépression au VIH a été retrouvée dans 14%. Un dispositif invasif était présent dans 93% des cas. Les prélèvements microbiologiques réalisés étaient : un examen cytobactériologique des urines (36 cas), un prélèvement de pus (19 cas), une hémoculture (23 cas). Les infections étaient urinaires (30 cas), du site opératoire (16 cas), une bactériémie (15 cas), une pneumopathie acquise sous ventilation mécanique (2 cas). Un germe était isolé dans ces prélèvements dans 94,4%. Les germes retrouvés étaient des entérobactéries (33 cas), des bacilles à Gram négatif non fermentant (12 cas), des cocci à Gram positif (6 cas) et des levures (3 cas). L’écologie était dominée par une résistance élevée des germes impliqués dans ces infections. Conclusion : Ce travail a montré une prévalence élevée des infections nosocomiales avec un profil de résistance varié des germes impliqués. Il est important d'élargir ce travail afin d'en tirer des recommandations fortes.

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Usman, S. O., O. M. Ajayi, O. Ebiekura, N. Egbonrelu, G. Ebhojie, and A. O. Ariyo. "Evidence of virological failure in patients on second-line anti-retroviral therapy in Southwestern Nigeria: An indication for HIV drug resistance testing." African Journal of Clinical and Experimental Microbiology 22, no. 3 (July 2, 2021): 415–19. http://dx.doi.org/10.4314/ajcem.v22i3.13.

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Background: In sub-Saharan Africa where genotypic anti-retroviral (ARV) drug resistance testing is rarely performed and poor adherence is blamed for the inability to achieve viral suppression and treatment failure, programmatic approaches to preventing and handling these are essential. This study was aimed at assessing the virological outcomes among HIV patients receiving second-line anti-retroviral therapy (ART) in Southwestern Nigeria.Methodology: This was a 5-year observational retrospective study of randomly selected people living with HIV (PLWHIV) who have been switched to second-line ART for at least six months before the commencement of the study in multiple comprehensive ART sites across the three levels of care, in Ondo and Ekiti States, Southwestern Nigeria, from January 2015 to December 2019. Quantitative viral load analysis was done using polymerase chain reaction (PCR) assay. Data were analyzed using the Statistical Package for Social Sciences (SPSS) version 24.0.Results: A total of 249 (71 males and 178 females) subjects eligible for the study were recruited using simple random sampling technique. The mean age (± SD) of the subjects was 44.21 ± 11.45 years. The mean number of years the patients have been on ART regimen was 7.92 ± 2.68 years. The mean number of years the patients were on first line ART regimen before being switched to second line was 4.27 ± 2.63 years. Patients with viral load <1000 RNA copies/ml (suppressed viral load) were 216 (86.7%) out of which 113 (45.4%) had viral load <20 RNA copies/ml while 33 (13.3%) had viral load >1000 RNA copies/ml (unsuppressed viral load or virological failure).Conclusion: About 13% of the patients on second line ART had unsuppressed viral load of more than 1000 RNA copies/ml indicating virological failure. Thus, critical factors such as poor adherence to ART and drug resistance chiefly contributing to virological failure have to be routinely checked. Keywords: suppression, ART, resistance, virological, failure, Nigeria French title: Preuve d'échec virologique chez les patients sous traitement antirétroviral de deuxième intention dans le sud-ouest du Nigeria: une indication pour le test de résistance aux médicaments contre le VIH Contexte: En Afrique subsaharienne, où les tests génotypiques de résistance aux antirétroviraux (ARV) sont rarement effectués et où une mauvaise observance est imputée à l'incapacité d'obtenir la suppression virale et l'échec du traitement, des approches programmatiques pour les prévenir et les gérer sont essentielles. Cette étude visait à évaluer les résultats virologiques chez les patients VIH recevant un traitement antirétroviral (TAR) de deuxième intention dans le sud-ouest du Nigeria. Méthodologie: Il s'agissait d'une étude rétrospective d'observation de 5 ans portant sur des personnes vivant avec le VIH (PVVIH) sélectionnées au hasard et passées à un TAR de deuxième intention pendant au moins six mois avant le début de l'étude dans plusieurs sites de TAR complets aux trois niveaux. de soins, dans les États d'Ondo et d'Ekiti, dans le sud-ouest du Nigéria, de janvier 2015 à décembre 2019. L'analyse quantitative de la charge virale a été effectuée à l'aide d'un test de réaction en chaîne par polymérase (PCR). Les données ont été analysées à l'aide du logiciel Paquet statistique pour les sciences sociales (SPSS) version 24.0. Résultats: Un total de 249 (71 hommes et 178 femmes) sujets éligibles à l'étude ont été recrutés à l'aide d'une technique d'échantillonnage aléatoire simple. L'âge moyen (± ET) des sujets était de 44,21±11,45 ans. Le nombre moyen d'années pendant lesquelles les patients ont été sous traitement antirétroviral était de 7,92±2,68 ans. Le nombre moyen d'années pendant lesquelles les patients étaient sous traitement antirétroviral de première ligne avant de passer en deuxième ligne était de 4,27 ± 2,63 ans. Les patients avec une charge virale <1000 copies d'ARN/ml (charge virale supprimée) étaient 216 (86,7%) dont 113 (45,4%) avaient une charge virale <20 copies d'ARN/ml tandis que 33 (13,3%) avaient une charge virale >1000 ARN copies/ml (charge virale non supprimée ou échec virologique). Conclusion: Environ 13 % des patients sous TAR de deuxième ligne avaient une charge virale non supprimée de plus de 1000 copies d'ARN/ml indiquant un échec virologique. Ainsi, les facteurs critiques tels qu'une mauvaise adhésion au TARV et la résistance aux médicaments contribuant principalement à l'échec virologique doivent être systématiquement vérifiés. Mots clés: suppression, TAR, résistance, virologique, échec, Nigeria

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Mathias, Clinton B., Jeffrey Rovatti, and Stephanie Polukort. "IL-10 enhances IgE-independent IL-33-mediated mast cell cytokine production." Journal of Immunology 198, no. 1_Supplement (May 1, 2017): 145.8. http://dx.doi.org/10.4049/jimmunol.198.supp.145.8.

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Abstract IgE antibodies play a critical role in antigen-mediated mast cell activation. However, mast cells can be activated via IgE-independent mechanisms including signaling via the IL-33 receptor ST2. We have previously shown that the Th2-derived cytokine IL-10 can enhance IgE-dependent mucosal mast cell activation and promote mast cell function and survival. However, whether the effects of IL-10 on mast cells are global in nature and not limited to IgE-mediated signaling is not clear. To determine whether IL-10 can prime the activation of mast cells mediated by IgE-independent signals such as IL-33, we assessed the effects of rIL-10 exposure on IL-33-stimulated mast cells and their subsequent activation via IgE. Bone marrow-derived mast cells (BMMCs) from wild-type (WT) and IL-10−/− mice were cultured with rIL-33 with or without rIL-10 and activated with DNP-IgE and antigen. Exposure to IL-10 enhanced cytokine production in both WT and IL-10−/− BMMCs, and this was significantly increased after activation via IgE. IL-10−/−BMMCs exhibited decreased cytokine production, but this was restored upon culture with rIL-10. Interestingly, IL-33 stimulation (and subsequent activation with IgE) induced comparably enhanced levels of cytokine production, specifically IL-13 and IL-6, in both WT and IL-10−/−cells, suggesting that ST2-mediated signals can overcome the lack of IL-10. However, the addition of exogenous IL-10 to IL-33-stimulated cultures further enhanced the levels of these cytokines not only in IgE-activated cells, but also in cells stimulated with IL-33 alone. Our observations therefore suggest that IL-10 can play critical roles in enhancing mast cell function both via IgE-dependent and independent mechanisms.

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Miller, Ashley M., Damo Xu, Darren L. Asquith, Laura Denby, Yubin Li, Naveed Sattar, Andrew H. Baker, Iain B. McInnes, and Foo Y. Liew. "IL-33 reduces the development of atherosclerosis." Journal of Experimental Medicine 205, no. 2 (February 11, 2008): 339–46. http://dx.doi.org/10.1084/jem.20071868.

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Atherosclerosis is a chronic inflammatory disease of the vasculature commonly leading to myocardial infarction and stroke. We show that IL-33, which is a novel IL-1–like cytokine that signals via ST2, can reduce atherosclerosis development in ApoE−/− mice on a high-fat diet. IL-33 and ST2 are present in the normal and atherosclerotic vasculature of mice and humans. Although control PBS-treated mice developed severe and inflamed atherosclerotic plaques in the aortic sinus, lesion development was profoundly reduced in IL-33–treated animals. IL-33 also markedly increased levels of IL-4, -5, and -13, but decreased levels of IFNγ in serum and lymph node cells. IL-33 treatment also elevated levels of total serum IgA, IgE, and IgG1, but decreased IgG2a, which is consistent with a Th1-to-Th2 switch. IL-33–treated mice also produced significantly elevated antioxidized low-density lipoprotein (ox-LDL) antibodies. Conversely, mice treated with soluble ST2, a decoy receptor that neutralizes IL-33, developed significantly larger atherosclerotic plaques in the aortic sinus of the ApoE−/− mice compared with control IgG-treated mice. Furthermore, coadministration of an anti–IL-5 mAb with IL-33 prevented the reduction in plaque size and reduced the amount of ox-LDL antibodies induced by IL-33. In conclusion, IL-33 may play a protective role in the development of atherosclerosis via the induction of IL-5 and ox-LDL antibodies.

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Park, Su-Ho, Myun Soo Kim, Hui Xuan Lim, Daeho Cho, and Tae Sung Kim. "IL-33-matured dendritic cells promote Th17 cell responses via IL-1β and IL-6." Cytokine 99 (November 2017): 106–13. http://dx.doi.org/10.1016/j.cyto.2017.07.022.

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Nagashima, Ryuichi, Hiroki Ishikawa, Yoshihiro Kuno, Chikara Kohda, and Masayuki Iyoda. "IL-33 attenuates renal fibrosis via group2 innate lymphoid cells." Cytokine 157 (September 2022): 155963. http://dx.doi.org/10.1016/j.cyto.2022.155963.

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Wang, J. X., S. Kaieda, S. Ameri, N. Fishgal, D. Dwyer, A. Dellinger, C. L. Kepley, M. F. Gurish, and P. A. Nigrovic. "IL-33/ST2 axis promotes mast cell survival via BCLXL." Proceedings of the National Academy of Sciences 111, no. 28 (June 30, 2014): 10281–86. http://dx.doi.org/10.1073/pnas.1404182111.

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Tsuji, Gaku, Akiko Hashimoto-Hachiya, Vu Hai Yen, Sho Miake, Masaki Takemura, Yasutaka Mitamura, Takamichi Ito, Maho Murata, Masutaka Furue, and Takeshi Nakahara. "Aryl Hydrocarbon Receptor Activation Downregulates IL-33 Expression in Keratinocytes via Ovo-Like 1." Journal of Clinical Medicine 9, no. 3 (March 24, 2020): 891. http://dx.doi.org/10.3390/jcm9030891.

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Background: IL-33, one of the IL-1 superfamily cytokines, has been shown to be associated with pruritus and inflammation in atopic dermatitis (AD). Furthermore, IL-33 production derived from keratinocytes reportedly has a crucial role in the development of AD; however, the mechanism of IL-33 expression has not been fully understood. Methods: We analyzed IL-33 expression in normal human epidermal keratinocytes (NHEKs) treated with IL-4. Results: IL-4 induced the upregulation of IL-33 expression in NHEKs. Based on the findings 1) that ovo-like 1 (OVOL1), a susceptible gene of AD, upregulates filaggrin (FLG) and loricrin (LOR) expression in NHEKs and 2) that reduced expression of FLG and LOR leads to production of IL-1 superfamily cytokines, we examined the involvement of OVOL1 in IL-33 expression in NHEKs. Knockdown of OVOL1 induced upregulation of IL-33 expression. Moreover, because Glyteer, an activator of aryl hydrocarbon receptor (AHR), reportedly upregulates OVOL1 expression, we examined whether treatment with Glyteer inhibited IL-33 expression in NHEKs. Treatment with Glyteer inhibited IL-4-induced upregulation of IL-33 expression, which was canceled by knockdown of either AHR or OVOL1. Conclusions: Activation of the AHR-OVOL1 axis inhibits IL-4-induced IL-33 expression, which could be beneficial for the treatment of AD.

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Duan, Lihua, Jie Chen, Feili Gong, and Guixiu Shi. "The Role of IL-33 in Rheumatic Diseases." Clinical and Developmental Immunology 2013 (2013): 1–5. http://dx.doi.org/10.1155/2013/924363.

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Interleukin-33 (IL-33), a novel member of IL-1 family, has been recently implicated in several inflammatory and autoimmune diseases. IL-33 can be produced by various types of tissues and cells and induce gene expression of Th2-associated cytokines via binding to the orphan receptor ST2. By promoting Th2 type immune response, IL-33 plays important roles in the allergy, whereas its function in autoimmune diseases attracts more attention. Recent studies reported the correlation of IL-33 with rheumatic diseases, and most of them found that the IL-33 expression levels were consistent with disease activity and development. Furthermore, evidence has indicated that IL-33-related treatment may ameliorate the pathogenic conditions and attenuate disease progression of those rheumatic diseases. Therefore, elucidation of the roles of IL-33 in rheumatic diseases would be beneficial to understand the pathogenesis and therapy of these diseases. In this paper, we will summarize the roles of IL-33 in the rheumatic diseases.

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Garth, Jaleesa M., Kristen M. Reeder, Joseph Mackel, Chad Dunaway, Jonathan Blackburn, and Chad Steele. "IL-33 signaling regulates innate IL-22 production via suppression of PGE2 during lung fungal infection." Journal of Immunology 198, no. 1_Supplement (May 1, 2017): 131.20. http://dx.doi.org/10.4049/jimmunol.198.supp.131.20.

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Abstract Members of the IL-1 family play both protective and regulatory roles in immune defense against the opportunistic mold Aspergillus fumigatus. Here, we investigated the role of the IL-1 family member IL-33 in lung defense after acute A. fumigatus exposure. IL-33 was detected in nanogram amounts in the naïve lung, which further increased after exposure to A. fumigatus in a Dectin-1 independent manner. Mice deficient in the receptor for IL-33 (IL-1RL1) unexpectedly demonstrated enhanced innate lung clearance of A. fumigatus. IL-33 functioned as a negative regulator of IL-22, as IL-22 was elevated in fungal-exposed Il1rl1−/− mice and IL-33 administration to normal mice attenuated fungal-induced IL-22 production. IL-33 mediated regulation of IL-22 did not involve the modulation of IL-23 but rather prostaglandin E2 (PGE2); PGE2 was significantly increased in fungal-exposed Il1rl1−/− mice and normal mice produced less PGE2 after fungal exposure when administered IL-33, suggesting that IL-33 mediated regulation of IL-22 occurred at the level of PGE2. This was confirmed by in vivo cyclooxygenase 2 (COX-2) inhibition and specific inhibition of PGE2 in vitro, both of which attenuated fungal-induced IL-22 in Il1rl1−/− mice. This study establishes novel mechanisms of IL-22 induction via PGE2 and regulation of the PGE2-IL-22 axis via IL-33 signaling during lung fungal exposure.

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Tsuji, Gaku, Kazuhiko Yamamura, Koji Kawamura, Makiko Kido-Nakahara, Takamichi Ito, and Takeshi Nakahara. "Regulatory Mechanism of the IL-33–IL-37 Axis via Aryl Hydrocarbon Receptor in Atopic Dermatitis and Psoriasis." International Journal of Molecular Sciences 24, no. 19 (September 27, 2023): 14633. http://dx.doi.org/10.3390/ijms241914633.

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Interleukin (IL)-33 and IL-37 have been identified as novel cytokines involved in various inflammatory diseases. However, their specific roles remain largely unknown. Recent studies have shown that IL-33, which triggers inflammation, and IL-37, which suppresses it, cooperatively regulate the balance between inflammation and anti-inflammation. IL-33 and IL-37 are also deeply involved in the pathogenesis of inflammatory skin diseases such as atopic dermatitis (AD) and psoriasis. Furthermore, a signaling pathway by which aryl hydrocarbon receptor (AHR), a receptor for dioxins, regulates the expression of IL-33 and IL-37 has been revealed. Here, we outline recent findings on the mechanisms regulating IL-33 and IL-37 expression in AD and psoriasis. IL-33 expression is partially dependent on mitogen-activated protein kinase (MAPK) activation, and IL-37 has a role in suppressing MAPK in human keratinocytes. Furthermore, IL-33 downregulates skin barrier function proteins including filaggrin and loricrin, thereby downregulating the expression of IL-37, which colocalizes with these proteins. This leads to an imbalance of the IL-33–IL-37 axis, involving increased IL-33 and decreased IL-37, which may be associated with the pathogenesis of AD and psoriasis. Therefore, AHR-mediated regulation of the IL-33–IL-37 axis may lead to new therapeutic strategies for the treatment of AD and psoriasis.

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Song, Yitian, Fangzhi Wei, Ying Liu, Feng Han, Lihui Ma, Yanping Zhuang, Chengdan Pan, Zhandong Jia, and Aimin Gong. "IL-33/ST2 Activation Is involved in Ro60-Regulated Photosensitivity in Cutaneous Lupus Erythematosus." Mediators of Inflammation 2022 (July 20, 2022): 1–15. http://dx.doi.org/10.1155/2022/4955761.

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Interleukin- (IL-) 33 contributes to various inflammatory processes. IL-33/ST2 activation participates in systemic lupus erythematous via binding to the receptor of Suppression of Tumorigenicity 2 protein (ST2). However, whether IL-33/ST2 interferes with the nosogenesis of cutaneous lupus erythematosus (CLE) has not been reported so far. Herein, we proposed to disclose the impacts on IL-33/ST2 activation and Ro60 on CLE and their potential implications in the photosensitization of CLE cells. IL-33, ST2, and Ro60 in CLE patients’ skin lesions were detected. Murine keratinocytes stimulated with or without IL-33 were irradiated by ultraviolet B (UVB), and the levels of Ro60 and inflammation markers were determined. Keratinocytes were cocultured with J774.2 macrophages and stimulated with IL-33 for analysis of chemostasis. The results identified that IL-33, ST2, and downstream inflammation markers were significantly upregulated in CLE lesions with Ro60 overexpression. Additionally, IL-33 treatment promoted the upregulation of Ro60 induced by UVB treatment in murine keratinocytes. Moreover, IL-33 stimulates keratinocytes to induce macrophage migration via enhancing the generation of the chemokine (C–C motif) ligands 17 and 22. Meanwhile, the silencing of ST2 or nuclear factor-kappa B (NF-κB) suppression abolished IL-33-induced upregulation of Ro60 in keratinocytes. Similarly, the inhibition of SOX17 expression was followed by downregulation of Ro60 in keratinocytes following IL-33 stimulation. In addition, UVB irradiation upregulated SOX17 in keratinocytes. Conclusively, the IL-33/ST2 axis interferes with Ro60-regulated photosensitization via activating the NF-κB- and PI3K/Akt- and SOX17-related pathways.

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Suzukawa, Maho, Motoyasu Iikura, Rikiya Koketsu, Hiroyuki Nagase, Chise Tamura, Akiko Komiya, Susumu Nakae, et al. "An IL-1 Cytokine Member, IL-33, Induces Human Basophil Activation via Its ST2 Receptor." Journal of Immunology 181, no. 9 (October 20, 2008): 5981–89. http://dx.doi.org/10.4049/jimmunol.181.9.5981.

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Chalubinski, Maciej, Katarzyna Wojdan, Emilia Luczak, Paulina Gorzelak, Maciej Borowiec, Adrian Gajewski, Karolina Rudnicka, Magdalena Chmiela, and Marlena Broncel. "IL-33 and IL-4 impair barrier functions of human vascular endothelium via different mechanisms." Vascular Pharmacology 73 (October 2015): 57–63. http://dx.doi.org/10.1016/j.vph.2015.07.012.

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Tsai, Mei-Lan, Ming-Kai Tsai, Yi-Giien Tsai, Yu-Chih Lin, Ya-Ling Hsu, Yi-Ting Chen, Yi-Ching Lin, and Chih-Hsing Hung. "Montelukast Increased IL-25, IL-33, and TSLP via Epigenetic Regulation in Airway Epithelial Cells." International Journal of Molecular Sciences 24, no. 2 (January 8, 2023): 1227. http://dx.doi.org/10.3390/ijms24021227.

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The epithelium-derived cytokines interleukin (IL)-25, IL-33, and thymic stromal lymphopoietin (TSLP) are important mediators that initiate innate type 2 immune responses in asthma. Leukotriene receptor antagonists (LTRAs) are commonly used to prevent asthma exacerbations. However, the effects of LTRAs on epithelium-derived cytokines expression in airway epithelial cells are unclear. This study aimed to investigate the effects of LTRAs on the expression of epithelium-derived cytokines in human airway epithelial cells and to explore possible underlying intracellular processes, including epigenetic regulation. A549 or HBE cells in air-liquid interface conditions were pretreated with different concentrations of LTRAs. The expression of epithelium-derived cytokines and intracellular signaling were investigated by real-time PCR, enzyme-linked immunosorbent assay, and Western blot. In addition, epigenetic regulation was investigated using chromatin immunoprecipitation analysis. The expression of IL-25, IL-33, and TSLP was increased under LTRAs treatment and suppressed by inhaled corticosteroid cotreatment. Montelukast-induced IL-25, IL-33, and TSLP expression were mediated by the mitogen-activated protein kinase (MAPK) and nuclear factor-κB (NF-κB) pathways and regulated by histone H3 acetylation and H3K36 and H3K79 trimethylation. LTRAs alone might increase inflammation and exacerbate asthma by inducing the production of IL-25, IL-33, and TSLP; therefore, LTRA monotherapy may not be an appropriate therapeutic option for asthma.

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YANGNGAM, SUPAPORN, SUYANEE THONGCHOT, KULTHIDA VAETEEWOOTTACHARN, PETI THUWAJIT, MARCELA A. HERMOSO, SEIJI OKADA, and CHANITRA THUWAJIT. "Intracellular IL-33 Attenuates Extracellular IL-33-induced Cholangiocarcinoma Cell Proliferation and Invasion via NF-κB and GSK-3β Pathways." Anticancer Research 41, no. 10 (September 30, 2021): 4917–28. http://dx.doi.org/10.21873/anticanres.15305.

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Duan, Lihua, Yan Huang, Qun Su, Qingyan Lin, Wen Liu, Jiao Luo, Bing Yu, et al. "Potential of IL-33 for Preventing the Kidney Injury via Regulating the Lipid Metabolism in Gout Patients." Journal of Diabetes Research 2016 (2016): 1–7. http://dx.doi.org/10.1155/2016/1028401.

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Interleukin-33 (IL-33), the most recently discovered member of the IL-1 superfamily, has been linked to several human pathologies including autoimmune diseases, sepsis, and allergy through its specific IL-1 receptor ST2. However, there is little information regarding the role of IL-33 in gout. In this study, we investigated the potential role of IL-33 in gout patients. The serum level of IL-33 was measured by ELISA, and the clinical and laboratory parameters, serum creatinine, urea, and lipid, were extracted from medical record system. The serum IL-33 expression was predominantly increased in gout patients compared to healthy controls, and the IL-33 levels were higher in patients without kidney injury. Furthermore, IL-33 showed a negative correlation with biomarkers of kidney injury, such as CRE and urea. The lipid metabolism dysfunction, tophi, and hypertension are the common reasons for kidney injury in gout. Interestingly, inverse and positive correlation of IL-33 expression was observed in LDL and HDL, respectively. However, there was no significant alteration in the gout patients with hypertension and tophi. These data suggested that IL-33 might act as a protective role in kidney injury through regulating the lipid metabolism in gout.

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Duez, Catherine, Barbara Gross, Philippe Marquillies, Valérie Ledroit, Bernhard Ryffel, and Corine Glineur. "Regulation of IL (Interleukin)-33 Production in Endothelial Cells via Kinase Activation and Fas/CD95 Upregulation." Arteriosclerosis, Thrombosis, and Vascular Biology 40, no. 11 (November 2020): 2619–31. http://dx.doi.org/10.1161/atvbaha.120.314832.

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Objective: The occurrence of new blood vessel formation in the lungs of asthmatic patients suggests a critical role for airway endothelial cells (ECs) in the disease. IL-33 (Interleukin-33)—a cytokine abundantly expressed in human lung ECs—recently emerged as a key factor in the development of allergic diseases, including asthma. In the present study, we evaluated whether mouse and human ECs exposed to the common Dermatophagoides farinae allergen produce IL-33 and characterized the activated signaling pathways. Approach and Results: Mouse primary lung ECs were exposed in vitro to D farinae extract or rmIL-33 (recombinant murine IL-33). Both D farinae and rmIL-33 induced Il-33 transcription without increasing the IL-33 production and upregulated the expression of its receptor, as well as genes involved in angiogenesis and the regulation of immune responses. In particular, D farinae and rmIL-33 upregulated Fas/Cd95 transcript level, yet without promoting apoptosis. Inhibition of caspases involved in the Fas signaling pathway, increased IL-33 protein level in ECs, suggesting that Fas may decrease IL-33 level through caspase-8-dependent mechanisms. Our data also showed that the NF-κB (nuclear factor-κB), PI3K/Akt, and Wnt/β-catenin pathways regulate Il-33 transcription in both mouse and human primary ECs. Conclusions: Herein, we described a new mechanism involved in the control of IL-33 production in lung ECs exposed to allergens.

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Mahlakõiv, T., A. L. Flamar, L. K. Johnston, S. Moriyama, G. G. Putzel, P. J. Bryce, and D. Artis. "Stromal cells maintain immune cell homeostasis in adipose tissue via production of interleukin-33." Science Immunology 4, no. 35 (May 3, 2019): eaax0416. http://dx.doi.org/10.1126/sciimmunol.aax0416.

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Obesity is driven by chronic low-grade inflammation resulting from dysregulated immune cell accumulation and function in white adipose tissue (WAT). Interleukin-33 (IL-33) is a key cytokine that controls innate and adaptive immune cell activity and immune homeostasis in WAT, although the sources of IL-33 have remained controversial. Here, we show that WAT-resident mesenchyme-derived stromal cells are the dominant producers of IL-33. Adipose stem and progenitor cells (ASPCs) produced IL-33 in all WAT depots, whereas mesothelial cells served as an additional source of IL-33 in visceral WAT. ASPC-derived IL-33 promoted a regulatory circuit that maintained an immune tone in WAT via the induction of group 2 innate lymphoid cell–derived type 2 cytokines and maintenance of eosinophils, whereas mesothelial IL-33 also acted as an alarmin by inducing peritoneal immune response upon infection. Together, these data reveal a previously unrecognized regulatory network between tissue-resident progenitor cells and innate lymphoid cells that maintains immune homeostasis in adipose tissue.

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Suzukawa, Maho, Masao Yamaguchi, Motoyasu Iikura, Rikiya Koketsu, Akiko Komiya, Hiroyuki Nagase, Susumu Nakae, et al. "IL-33-induced activation of human basophils and eosinophils via ST2." Inflammation and Regeneration 30, no. 3 (2010): 181–85. http://dx.doi.org/10.2492/inflammregen.30.181.

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Hsu, Chia-Lin, and Paul Bryce. "IL-33 expression by mast cells is regulated by a Sphk-calcium-NFAT dependent pathway (117.5)." Journal of Immunology 186, no. 1_Supplement (April 1, 2011): 117.5. http://dx.doi.org/10.4049/jimmunol.186.supp.117.5.

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Abstract IL-33 is an IL-1 family cytokine that can act extracellularly via its receptor, T1/ST2 or intracellularly. Functionally, it promotes Th2-associated immunity by enhancing several cell type activation and survival. However, the regulation of IL-33 expression is still unclear. Previously, we showed that basal expression of IL-33 in mast cells was upregulated upon IgE activation. Ca2+ mobilization was sufficient and necessary to enhance IL-33 expression in mast cells. We wanted to further investigate the pathway that drives IL-33 expression. Two major Ca2+-dependent pathways induced in mast cells are inositol trisphosphate (IP3) bound to its receptor, IP3R, and sphingosine kinase 1/2 (Sphk1/2) generated sphingosine-1-phosphate (S1P). PI3K is the upstream regulator for Sphk1. Here, we demonstrate that inhibition of PI3K and Sphk activity decreases IL-33 expression via IgE activation while ionomycin stimulation, which bypasses the inhibition, restores IL-33 expression. Interruption of NFAT and calcineurin interaction, which is downstream of Ca2+ mobilization, also decreases IL-33 expression and ionomycin can not restore it. Blocking of IP3R or NF-kB does not influence IL-33 expression but inhibits another IL-1 family cytokine, IL-1b. In summary, IL-33 is upregulated upon cross-linking of IgE receptors on mast cells and expression is dependent on Ca2+ mobilization and regulated by a PI3K-Sphk1-NFAT pathway.

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Xiao, Yi, Feidi Chen, Ye Zhao, Mingming Sun, Xiangsheng Huang, Liang Chen, Suxia Yao, et al. "Interleukin-33 promotes REG3γ expression in intestinal epithelial cells via activation of mTOR, STAT3 and ERK1/2." Journal of Immunology 198, no. 1_Supplement (May 1, 2017): 200.12. http://dx.doi.org/10.4049/jimmunol.198.supp.200.12.

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Abstract REG3γ, an antimicrobial peptides typically expressed by intestinal epithelial cells (IEC), plays crucial roles in maintaining intestinal mucosal barrier functions against microbiota and potentially pathogenic microorganisms in the intestines. However, the mechanisms by which regulate IEC expression of REG3γ are still not fully understood. IL-33, a member of the IL-1 cytokine family, has been implicated in maintenance of intestinal homeostasis. In this study, we investigated whether and how IL-33 regulates IEC expression of REG3γ, thus contributes to the maintenance of intestinal homeostasis. We report here that the expression of REG3γ in IEC of IL-33−/− mice is significantly lower than that in the wild type (WT) mice at both mRNA and protein levels. Treatment with IL-33 induced IEC expression of REG3γ in mouse MSIE intestinal epithelial cell line. Consistently, IL-33 also induced expression of REG3α, the human ortholog of mouse REG3γ, in human epithelial cells. Mechanistically, rIL-33 activated phosphorylation of STAT3, mTOR and ERK1/2 in MSIE cells. Knockdown of STAT3, mTOR and ERK-activating enzyme MEK by using siRNA or CRISPR abrogated IL-33 induction of REG3γ expression in IEC, indicating that IL-33 promoted IEC expression of REG3γ though activating STAT3, mTOR and ERK1/2 pathways. REG3γ has been shown to be able kill gram-positive gut bacteria. Interestingly, total gut bacteria were significantly lower in IL-33−/− mice compared to WT mice, indicating that IL-33 regulation of gut microbiota, possibly through induction of IEC REG3γ. Put all together, our study demonstrated a novel crosstalk between IL-33 and REG3γ in maintenance of intestinal homeostasis.

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Liang, Yuejin, Panpan Yi, Zuliang Jie, Denley Denley Ming Kee Yuan, Lynn Soong, Yingzi Cong, and Jiaren Sun. "IL-33 promotes antiviral CD8+ T cells through the mTORC1 pathway and limits liver injury via recruiting immunosuppressive neutrophils." Journal of Immunology 198, no. 1_Supplement (May 1, 2017): 78.3. http://dx.doi.org/10.4049/jimmunol.198.supp.78.3.

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Abstract Viral hepatitis is a major public health problem worldwide. The multifunctional IL-33 is critical for the activity of antiviral cytotoxic T lymphocytes (CTLs) in persistent viral infection; however, the signaling mechanism defining how IL-33 promotes immune cell activation is unclear. In addition, IL-33 can also recruit neutrophils, suggesting that it may regulate liver injury through modulating myeloid cell functions. In this study, we revealed an essential role for endogenous IL-33 regarding antiviral T cell responses in lymphocytic choriomeningitis virus (LCMV) infection. Deficiency of CTL effector activity in IL-33 knockout (KO) mice was restored by recombinant IL-33 treatment. Mechanistically, IL-33 induced CD8+ T cell activation and proliferation through the PI3K/mTORC1 singling pathway. Interestingly, IL-33 treatment also induced significant neutrophil accumulation, but decreased CD8+ T cell numbers, in infected liver. By depleting neutrophils in vivo, we demonstrated that neutrophils played an immunomodulatory role and attenuated liver injury by inhibiting infiltration and the activity of CTLs at the contraction stage of immune response. IL-33-induced immunosuppressive neutrophils expressed higher levels of arginase-1 through type 2 innate lymphoid cells (ILC2)/IL-13/STAT6 axis. This study, therefore, demonstrates a dual role of IL-33 in promoting antiviral CD8+ T cell response at the initial stage, but inducing immunomodulatory neutrophils through induction of ILC2 to limit liver injury during the contraction stage of immune response.

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Reichenbach, Dawn K., Vincent Schwarze, Benjamin M. Matta, Victor Tkachev, Elizabeth Lieberknecht, Quan Liu, Brent H. Koehn, et al. "Regulation of Immune Responses during Acute GvHD Via the IL-33/ST2 Axis." Blood 124, no. 21 (December 6, 2014): 844. http://dx.doi.org/10.1182/blood.v124.21.844.844.

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Abstract The IL-1 superfamily member IL-33 is produced in barrier tissues. IL-33 binds to the receptor suppression of tumorigenicity 2 (ST2), expressed on stromal cells, regulatory T cells (Tregs), myeloid derived suppressor cells (MDSCs), and macrophages. IL-33 has both anti-inflammatory and pro-inflammatory properties. It is not known if IL-33 plays a role in acute GvHD, and if so what properties it exerts. By immunohistochemistry staining of gut tissues, IL-33 production by non-hematopoietic cells was increased in mice post-conditioning and in patients during GvHD. To determine whether IL-33 could augment GvHD via a host signaling mechanism, we compared st2-/-to wildtype (wt) hosts and observed decreased GvHD lethality (Figure 1A). Additionally, IL-33-/- versus wt hosts had a marked decrease in GvHD lethality and reduced TNFα production. Conversely, IL-33 administration during the peak inflammatory response worsened GvHD. Previous studies have shown increased levels of the soluble form of ST2 (sST2) are a biomarker for steroid-refractory GvHD (Vander Lugt, NEJM, 2013). We hypothesized that sST2 acted not only as an indicator of tissue injury and biomarker of GvHD but also as an immune modulator during GvHD. In rodents, we found that ST2 was upregulated on alloreactive T cells and sST2 increased as GvHD progressed. St2-/-versus wt donor T cells had a marked reduction in GvHD lethality (Figure 1B) without compromise of graft-vs-leukemia responses. Comparable data was seen in 2 different strain combinations. Alloantigen-induced IL-18 receptor upregulation was significantly lower in the absence of ST2, which was linked to significantly reduced IFNγ production by st2-/- vs wt CD4 and CD8 T cells during GvHD. Similarly, sST2 transgenic hosts and wt recipients given exogenous sST2-Fc fusion protein infusions (Figure 1C) to block ST2/IL-33 interaction each had significantly reduced GVHD lethality, establishing the functional role of ST2 as a decoy receptor modulating GVHD. During the peak of the GvHD inflammatory response, IL-33 signalling of either donor or host cells promoted activation of donor T cells, while the use of exogenous sST2-Fc protein to prevent IL33/ST2 engagement ameliorates disease. Together, these studies point to targeting of the IL-33/ST2 axis as a novel and potent target for GvHD therapy. Disclosures Warncke: Novartis Pharma AG: Employment. Junt:Novartis Pharma AG: Employment.

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Saxton, Sophie N., Alice S. Whitley, Ryan J. Potter, Sarah B. Withers, Richard Grencis, and Anthony M. Heagerty. "Interleukin-33 rescues perivascular adipose tissue anticontractile function in obesity." American Journal of Physiology-Heart and Circulatory Physiology 319, no. 6 (December 1, 2020): H1387—H1397. http://dx.doi.org/10.1152/ajpheart.00491.2020.

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In this study, we have shown that administering IL-33 to obese mice will restore PVAT anticontractile function, and this is accompanied by normalized blood pressure, blood glucose, and plasma insulin. Moreover, the PVAT effect is enhanced in control mice given IL-33. IL-33 induced a hypereosinophilic phenotype in our mice, and the effects of IL-33 on PVAT function, blood pressure, and blood glucose are absent in eosinophil-deficient mice, suggesting that the effects of IL-33 are mediated via eosinophils.

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Waddell, Amanda, Jefferson E. Vallance, Amy Hummel, Theresa Alenghat, and Michael J. Rosen. "IL-33 Induces Murine Intestinal Goblet Cell Differentiation Indirectly via Innate Lymphoid Cell IL-13 Secretion." Journal of Immunology 202, no. 2 (December 7, 2018): 598–607. http://dx.doi.org/10.4049/jimmunol.1800292.

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Dai, Xiuju, Mikiko Tohyama, Masamoto Murakami, Yasushi Hanakawa, and Koji Sayama. "House dust mite allergen releases IL-31 and IL-33 from epidermal keratinocytes via ATP signaling." Journal of Dermatological Science 84, no. 1 (October 2016): e70-e71. http://dx.doi.org/10.1016/j.jdermsci.2016.08.218.

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Cheng, Li, Yang Jiao, Wei Jiang, Xin Zhang, Liping Zhang, and Gongwei Jia. "IL-33 Deficiency Attenuates Lung Inflammation by Inducing Th17 Response and Impacting the Th17/Treg Balance in LPS-Induced ARDS Mice via Dendritic Cells." Journal of Immunology Research 2022 (December 16, 2022): 1–12. http://dx.doi.org/10.1155/2022/9543083.

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Objectives. The characteristic pathophysiological feature of acute respiratory distress syndrome (ARDS) is a dysregulated inflammatory response. T helper 17 (Th17) cells in the lung are inflammatory cells that contribute to pulmonary inflammatory cascades. In addition, Th17/regulatory T cells (Treg cells) also play an important role in the inflammatory process. Dendritic cells (DCs) can regulate the differentiation of CD4+ T cells, including Th17 and Treg cells. Recent evidence revealed that interleukin-33 (IL-33) signaling could activate and mature DCs. Therefore, the aim of this study was to investigate the effects of IL-33 on inflammation and immunoregulation by inducing the Th17 response and influencing the Th17/Treg balance in LPS-induced ARDS. Methods. IL-33 gene knockout mice and the administration of recombinant mouse IL-33 (rmIL-33) were used to investigate the role of IL-33 and the underlying mechanisms in an LPS-induced ARDS model. Hematoxylin and eosin (H&E) staining, wet/dry (W/D) weight ratios, cell counts, and the levels of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), interleukin-6 (IL-6), interleukin-17 (IL-17), and interleukin-10 (IL-10) in bronchoalveolar lavage fluid (BALF) were investigated. The levels of IL-33, orphan nuclear receptor gamma t (RORγt), and forkhead transcription factor protein 3 (FOXP3) protein in lung tissue were evaluated by Western blotting. The mRNA expression levels of IL-33 and RORγt were measured by quantitative real-time polymerase chain reaction (qRT-PCR). Th17 and Treg cell frequencies were determined by flow cytometry. The levels of IL-6 in the supernatant in a dendritic cell culture system were examined by ELISA. Results. Increased expression of IL-33 was observed in mice with LPS-induced ARDS. IL-33 deficiency significantly inhibited inflammation and attenuated LPS-induced ARDS, whereas pretreatment with rmIL-33 aggravated pulmonary inflammatory response. Furthermore, depletion of IL-33 inhibited Th17 cells, significantly decreased RORγt mRNA and protein expression and IL-17 levels in BALF, and led to less differentiation of T cells into Th17 cells than Treg cells. Moreover, IL-33-/- DCs secreted less IL-6 and IL-23 than normal control DCs. Conclusion. IL-33 deficiency alleviated lung injury in the LPS-induced ARDS model, which was closely related to suppressing Th17 responses and regulating the Th17/Treg balance. The expansion of Th17 cells and imbalance in Th17/Treg cells may be associated with IL-6 and IL-23 secreted from IL-33-activated DCs.

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Dagher, Rania, Alan M. Copenhaver, Valerie Besnard, Marielle Maret, Fatima Hamidi, Aaron A. Berlin, Michel Aubier, Roland Kolbeck, Alison A. Humbles, and Marina Pretolani. "IL-33/ST2 macrophage crosstalk promotes lung epithelial repair." Journal of Immunology 198, no. 1_Supplement (May 1, 2017): 211.13. http://dx.doi.org/10.4049/jimmunol.198.supp.211.13.

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Abstract Increasing evidence points to a central role for macrophages in tissue regeneration, however, the molecular mechanisms underlying this function remain unknown. Here, using depletion and adoptive transfer approaches, we demonstrate a major role of alveolar macrophages in facilitating bronchial re-epithelialization. In addition, we identify a novel, and paradoxical, protective role for the IL-33/ST2 axis in epithelial repair following naphthalene (NA)-induced lung injury. We defined two subsets of ST2 expressing myeloid cells, namely recruited monocyte-derived cells and resident alternatively activated macrophages (AAMs), which infiltrate the airways during the regeneration of the bronchial epithelium. Further, ST2-deficient mice exhibited an incomplete epithelial repair which was associated with a dysfunctional AAM phenotype and a reduction in the proliferation of a self-renewing subset of Clara progenitor stem cells. Notably, reconstitution of ST2+ AAMs, post NA, completely restored the epithelium in ST2-deficient animals. In contrast, the monocyte/macrophage-dependent CCL2/CCR2 axis was redundant for repair, however, anti ST2-antibody treatment to CCR2−/− mice resulted in ineffective epithelial regeneration and confirmed the observations seen with ST2-deficiency after NA-induced injury. Thus, the IL-33/ST2 pathway regulates effective Clara cell regeneration and bronchial re-epithelialization via AAM polarization and may lead to new therapeutic insights in acute respiratory diseases.

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Yang, Fuhan, Mingming Wen, Dayu Pan, Xian Lin, Jing Mo, Xueyi Dong, Shihan Liao, and Yuemei Ma. "IL-33/ST2 Axis Regulates Vasculogenic Mimicry via ERK1/2-MMP-2/9 Pathway in Melanoma." Dermatology 235, no. 3 (2019): 225–33. http://dx.doi.org/10.1159/000498857.

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Background: Melanoma, an extremely malignant form of cancer, poses a significant health risk. Vasculogenic mimicry (VM), blood vessels formed by tumor cells instead of endothelial cells, is an important factor for the rapid progression of melanoma. Interleukin (IL)-33 is an inflammatory factor commonly found in the tumor microenvironment and plays an important role in the progression of many tumors. IL-33 acts on immune cells and tumor cells through its receptor ST2. This study hypothesized that IL-33 directly affects the progression of melanoma. Objectives: This study was designed to investigate the effect of IL-33 on VM of melanoma and its potential mechanism of action. Methods: The expression of ST2 was evaluated in 66 cases of melanoma collected from human patients, and the differences were analyzed. In vitro experiments were conducted to study the effects of the IL-33/ST2 axis on cell migration and invasion and to elucidate possible mechanisms. Results: ST2 expression is associated with that of matrix metalloproteinase (MMP)-2 and VM in melanoma of patients. IL-33 increases the abilities of proliferation, migration and invasion of melanoma cells and VM tube formation through ST2. IL-33 induces the production of MMP-2/9 via ERK1/2 phosphorylation. Conclusion: IL-33 can directly act on melanoma cells and promote its development.

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Mohd Jaya, Fatin Nurizzati, Zhongyi Liu, and Godfrey Chi-Fung Chan. "Early Treatment of Interleukin-33 can Attenuate Lupus Development in Young NZB/W F1 Mice." Cells 9, no. 11 (November 10, 2020): 2448. http://dx.doi.org/10.3390/cells9112448.

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Interleukin-33 (IL-33), a member of the IL-1 cytokine family, has been recently associated with the development of autoimmune diseases, including systemic lupus erythematosus (SLE). IL-33 is an alarmin and a pleiotropic cytokine that affects various types of immune cells via binding to its receptor, ST2. In this study, we determine the impact of intraperitoneal IL-33 treatments in young lupus, NZB/W F1 mice. Mice were treated from the age of 6 to 11 weeks. We then assessed the proteinuria level, renal damage, survival rate, and anti-dsDNA antibodies. The induction of regulatory B (Breg) cells, changes in the level of autoantibodies, and gene expression were also examined. In comparison to the control group, young NZB/W F1 mice administered with IL-33 had a better survival rate as well as reduced proteinuria level and lupus nephritis. IL-33 treatments significantly increased the level of IgM anti-dsDNA antibodies, IL-10 expressing Breg cells, and alternatively-induced M2 macrophage gene signatures. These results imply that IL-33 exhibits a regulatory role during lupus onset via the expansion of protective IgM anti-dsDNA as well as regulatory cells such as Breg cells and M2 macrophages.

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Zhao, Qing, and Guangjie Chen. "Role of IL-33 and Its Receptor in T Cell-Mediated Autoimmune Diseases." BioMed Research International 2014 (2014): 1–10. http://dx.doi.org/10.1155/2014/587376.

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Interleukin-33 (IL-33) is a new cytokine of interleukin-1 family, whose specific receptor is ST2. IL-33 exerts its functions via its target cells and plays different roles in diseases. ST2 deletion and exclusion of IL-33/ST2 axis are accompanied by enhanced susceptibility to dominantly T cell-mediated organ-specific autoimmune diseases. It has been reported that IL-33/ST2 pathway plays a key role in host defense and immune regulation in inflammatory and infectious diseases. This review focuses on new findings in the roles of IL-33 and ST2 in several kinds of T cell-mediated autoimmune diseases.

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Meiners, Jana, Martina Reitz, Nikolas Rüdiger, Jan-Eric Turner, Lennart Heepmann, Lena Rudolf, Wiebke Hartmann, Henry J. McSorley, and Minka Breloer. "IL-33 facilitates rapid expulsion of the parasitic nematode Strongyloides ratti from the intestine via ILC2- and IL-9-driven mast cell activation." PLOS Pathogens 16, no. 12 (December 22, 2020): e1009121. http://dx.doi.org/10.1371/journal.ppat.1009121.

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Parasitic helminths are sensed by the immune system via tissue-derived alarmins that promote the initiation of the appropriate type 2 immune responses. Here we establish the nuclear alarmin cytokine IL-33 as a non-redundant trigger of specifically IL-9-driven and mast cell-mediated immunity to the intestinal parasite Strongyloides ratti. Blockade of endogenous IL-33 using a helminth-derived IL-33 inhibitor elevated intestinal parasite burdens in the context of reduced mast cell activation while stabilization of endogenous IL-33 or application of recombinant IL-33 reciprocally reduced intestinal parasite burdens and increased mast cell activation. Using gene-deficient mice, we show that application of IL-33 triggered rapid mast cell-mediated expulsion of parasites directly in the intestine, independent of the adaptive immune system, basophils, eosinophils or Gr-1+ cells but dependent on functional IL-9 receptor and innate lymphoid cells (ILC). Thereby we connect the described axis of IL-33-mediated ILC2 expansion to the rapid initiation of IL-9-mediated and mast cell-driven intestinal anti-helminth immunity.

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Still, Katherine M., Samantha J. Batista, Carleigh A. O’Brien, Oyebola O. Oyesola, Simon P. Früh, Lauren M. Webb, Igor Smirnov, et al. "Astrocytes promote a protective immune response to brain Toxoplasma gondii infection via IL-33-ST2 signaling." PLOS Pathogens 16, no. 10 (October 27, 2020): e1009027. http://dx.doi.org/10.1371/journal.ppat.1009027.

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It is of great interest to understand how invading pathogens are sensed within the brain, a tissue with unique challenges to mounting an immune response. The eukaryotic parasite Toxoplasma gondii colonizes the brain of its hosts, and initiates robust immune cell recruitment, but little is known about pattern recognition of T. gondii within brain tissue. The host damage signal IL-33 is one protein that has been implicated in control of chronic T. gondii infection, but, like many other pattern recognition pathways, IL-33 can signal peripherally, and the specific impact of IL-33 signaling within the brain is unclear. Here, we show that IL-33 is expressed by oligodendrocytes and astrocytes during T. gondii infection, is released locally into the cerebrospinal fluid of T. gondii-infected animals, and is required for control of infection. IL-33 signaling promotes chemokine expression within brain tissue and is required for the recruitment and/or maintenance of blood-derived anti-parasitic immune cells, including proliferating, IFN-γ-expressing T cells and iNOS-expressing monocytes. Importantly, we find that the beneficial effects of IL-33 during chronic infection are not a result of signaling on infiltrating immune cells, but rather on radio-resistant responders, and specifically, astrocytes. Mice with IL-33 receptor-deficient astrocytes fail to mount an adequate adaptive immune response in the CNS to control parasite burden–demonstrating, genetically, that astrocytes can directly respond to IL-33 in vivo. Together, these results indicate a brain-specific mechanism by which IL-33 is released locally, and sensed locally, to engage the peripheral immune system in controlling a pathogen.

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Tembhre, Manoj Kumar, Mukesh Kumar Sriwastva, Milind Padmakar Hote, Shikha Srivastava, Priyanka Solanki, Shafaque Imran, Ramakrishnan Lakshmy, Alpana Sharma, Kailash Jaiswal, and Ashish Datt Upadhyay. "Interleukin-33 Induces Neutrophil Extracellular Trap (NET) Formation and Macrophage Necroptosis via Enhancing Oxidative Stress and Secretion of Proatherogenic Factors in Advanced Atherosclerosis." Antioxidants 11, no. 12 (November 26, 2022): 2343. http://dx.doi.org/10.3390/antiox11122343.

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Interleukin-33 (IL-33) acts as an ‘alarmin’, and its role has been demonstrated in driving immune regulation and inflammation in many human diseases. However, the precise mechanism of action of IL-33 in regulating neutrophil and macrophage functioning is not defined in advanced atherosclerosis (aAT) patients. Further, the role of IL-33 in neutrophil extracellular trap (NET) formation in aAT and its consequent effect on macrophage function is not known. In the present study, we recruited n = 52 aAT patients and n = 52 control subjects. The neutrophils were isolated from both groups via ficoll/percoll-based density gradient centrifugation. The effect of IL-33 on the NET formation ability of the neutrophils was determined in both groups. Monocytes, isolated via a positive selection method, were used to differentiate them into macrophages from each of the study subjects and were challenged by IL-33-primed NETs, followed by the measurement of oxidative stress by calorimetric assay and the expression of the proinflammatory molecules by quantitative PCR (qPCR). Transcript and protein expression was determined by qPCR and immunofluorescence/ELISA, respectively. The increased expression of IL-33R (ST-2) was observed in the neutrophils, along with an increased serum concentration of IL-33 in aAT compared to the controls. IL-33 exacerbates NET formation via specifically upregulating CD16 expression in aAT. IL-33-primed NETs/neutrophils increased the cellular oxidative stress levels in the macrophages, leading to enhanced macrophage necroptosis and the release of atherogenic factors and matrix metalloproteinases (MMPs) in aAT compared to the controls. These findings suggested a pathogenic effect of the IL-33/ST-2 pathway in aAT patients by exacerbating NET formation and macrophage necroptosis, thereby facilitating the release of inflammatory factors and the release of MMPs that may be critical for the destabilization/rupture of atherosclerotic plaques in aAT. Targeting the IL-33/ST-2-NETs axis may be a promising therapeutic target for preventing plaque instability/rupture and its adverse complications in aAT.

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Chen, Zuojia, Jialie Luo, Jian Li, Girak Kim, Andy Stewart, Yuefeng Huang, and Chuan Wu. "Intestinal IL-33 promotes platelet activity for neutrophil recruitment during acute inflammation." Blood 139, no. 12 (March 24, 2022): 1878–91. http://dx.doi.org/10.1182/blood.2021013474.

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Abstract Peripheral serotonin (5-HT) is mainly generated from the gastrointestinal tract and taken up and stored by platelets in the circulation. Although the gut is recognized as a major immune organ, how intestinal local immune responses control whole-body physiology via 5-HT remains unclear. Here, we show that intestinal inflammation enhances systemic platelet activation and blood coagulation. Intestinal epithelium damage induces elevated levels of the alarm cytokine interleukin-33 (IL-33), leading to platelet activation via promotion of gut-derived 5-HT release. More importantly, we found that loss of intestinal epithelial-derived IL-33 lowers peripheral 5-HT levels, resulting in compromised platelet activation and hemostasis. Functionally, intestinal IL-33 contributes to the recruitment of neutrophils to sites of acute inflammation by enhancing platelet activities. Genetic deletion of intestinal IL-33 or neutralization of peripheral IL-33 protects animals from lipopolysaccharide endotoxic shock through attenuated neutrophil extravasation. Therefore, our data establish a distinct role of intestinal IL-33 in activating platelets by promoting 5-HT release for systemic physiology and inflammation.

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Lv, Ran, Jinning Zhao, Min Lei, Dongju Xiao, Yijin Yu, and Junran Xie. "IL-33 Attenuates Sepsis by Inhibiting IL-17 Receptor Signaling through Upregulation of SOCS3." Cellular Physiology and Biochemistry 42, no. 5 (2017): 1961–72. http://dx.doi.org/10.1159/000479836.

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Background/Aims: Sepsis is a systemic inflammatory response during infection. There are limited therapeutic options for sepsis patients. Interleukin (IL)-33 has been reported recently with a beneficial effect in mouse sepsis. Methods: In this study, we initiated a clinical study to measure serum levels of pro-inflammatory cytokines including IL-33 in sepsis patients. Next, we employed cecal ligation and puncture (CLP) to study the role of IL-33 during sepsis. To further dissect the molecular mechanism, we used in vivo knockout models and in vitro knockdown murine embryonic fibroblasts (MEFs) to investigate the cross-talk between IL-33 and IL-17 signaling, and to identify the potential downstream mediators. Results: IL-33 and IL-17 were upregulated in both clinical and experimental sepsis. In CLP, IL-33 (-/-) mice showed higher mortality rate, and IL-33 treatment improved the survival rate. Elevated proinflammatory cytokines in sepsis were related to IL-17 from γδT cells. IL-33 treatment suppressed production of these cytokines by targeting IL-17 signaling both in vivo and in vitro. Finally, IL-33 was shown to inhibit the IL-17 pathway via activating suppressor of cytokine signaling (SOCS)-3. Conclusion: Collectively, the results suggest that IL-33 plays a negative regulatory role in sepsis progression by inhibiting IL-17 pathway through activating SOCS3. This finding would inspire a new therapeutic strategy for treating sepsis.

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Lin, Yu-Chun, Wen-Yen Huang, Tsai-Yu Lee, Yi-Ming Chang, Su-Feng Chen, Yaoh-Shiang Lin, and Shin Nieh. "Interleukin-33-Enhanced CXCR4 Signaling Circuit Mediated by Carcinoma-Associated Fibroblasts Promotes Invasiveness of Head and Neck Cancer." Cancers 13, no. 14 (July 9, 2021): 3442. http://dx.doi.org/10.3390/cancers13143442.

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Despite recent advances, treatment for head and neck squamous cell carcinoma (HNSCC) has limited efficacy in preventing tumor progression. We confirmed previously that carcinoma-associated fibroblasts (CAF)-induced interleukin-33 (IL-33) contributed to cancer progression. However, the molecular mechanisms underlying the complex communication network of the tumor microenvironment merited further evaluation. To simulate the IL-33-induced autocrine signaling, stable clones of IL-33-overexpressing HNSCC cells were established. Besides well-established IL-33/ST2 and SDF1/CXCR4 (stromal-derived factor 1/C-X-C motif chemokine receptor 4) signaling, the CAF-induced IL-33 upregulated CXCR4 via cancer cell induction of IL-33 self-production. The IL-33-enhanced-CXCR4 regulatory circuit involves SDF1/CXCR4 signaling activation and modulates tumor behavior. An in vivo study confirmed the functional role of IL-33/CXCR4 in tumor initiation and metastasis. The CXCR4 and/or IL-33 blockade reduced HNSCC cell aggressiveness, with attenuated invasions and metastases. Immunohistochemistry confirmed that IL-33 and CXCR4 expression correlated significantly with disease-free survival and IL-33-CXCR4 co-expression predicted a poor outcome. Besides paracrine signaling, the CAF-induced IL-33 reciprocally enhanced the autocrine cancer-cell self-production of IL-33 and the corresponding CXCR4 upregulation, leading to the activation of SDF1/CXCR4 signaling subsequent to cancer progression. Thus, targeting the IL-33-enhanced-CXCR4 regulatory circuit attenuates tumor aggressiveness and provides a potential therapeutic option for improving the prognosis in HNSCC patients.

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Umebashi, Katsuyuki, Masayoshi Yamamoto, Akinori Tokito, Ku Sudou, Yoko Takenoshita, and Michihisa Jougasaki. "Inhibitory Effects of Simvastatin on IL-33-Induced MCP-1 via the Suppression of the JNK Pathway in Human Vascular Endothelial Cells." International Journal of Molecular Sciences 24, no. 16 (August 21, 2023): 13015. http://dx.doi.org/10.3390/ijms241613015.

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An alarmin, interleukin (IL)-33 is a danger signal that causes inflammation, inducing chemotactic proteins such as monocyte chemoattractant protein (MCP)-1 in various cells. As statins have pleiotropic actions including anti-inflammatory properties, we investigated the effects of simvastatin on IL-33-induced MCP-1 expression in human umbilical vein endothelial cells (HUVECs). HUVECs were stimulated with IL-33 in the presence or absence of simvastatin. Gene expression and protein secretion of MCP-1, phosphorylation of mitogen-activated protein kinase (MAPK), nuclear translocation of phosphorylated c-Jun, and human monocyte migration were investigated. Immunocytochemical staining and Western immunoblot analysis revealed that IL-33 augmented MCP-1 protein expression in HUVECs. Real-time reverse transcription–polymerase chain reaction (RT-PCR) and enzyme-linked immunosorbent assay (ELISA) showed that IL-33 significantly increased MCP-1 mRNA and protein secretion, which were suppressed by c-jun N-terminal kinase (JNK) inhibitor SP600125 and p38 MAPK inhibitor SB203580. Simvastatin inhibited IL-33-induced MCP-1 mRNA, protein secretion, phosphorylation of JNK and c-Jun. Additionally, the IL-33-induced nuclear translocation of phosphorylated c-Jun and THP-1 monocyte migration were also blocked by simvastatin. This study demonstrated that IL-33 induces MCP-1 expression via the JNK and p38 MAPK pathways in HUVECs, and that simvastatin inhibits MCP-1 production by selectively suppressing JNK. Simvastatin may inhibit the progression of IL-33-induced inflammation via suppressing JNK to prevent MCP-1 production.

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Li, Shu, Feng-xue Zhu, Hong-bin Zhang, Hui Li, and You-zhong An. "Pretreatment with interleukin-33 reduces warm hepatic ischemia/reperfusion injury in mice." Chinese Medical Journal 126, no. 10 (May 20, 2013): 1855–59. http://dx.doi.org/10.3760/cma.j.issn.0366-6999.20123530.

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Background Interleukin (IL)-33 is a recently identified member of the IL-1 family that binds to the receptor, ST2L. This study examined IL-33 production in mouse liver and investigated its role in hepatic ischemia/reperfusion (I/R) injury. Methods Male BALB/c mice ((22±3) g) were subjected to 90 minutes partial hepatic ischemia, followed by 6 hours reperfusion. First, mice were randomized into two groups: control group (laparotomy only, without blocking blood supply) and ischemia model group. IL-33 mRNA and serum protein levels were measured at 30, 60, 90 minutes after ischemia and 2 and 6 hours after reperfusion. Second, mice were randomized into four groups: control, model (injection of rabbit IgG polyclonal antibody), recombinant IL-33 intervention and anti-ST2L antibody intervention group. Mice were sacrificed 6 hours after reperfusion. Liver pathology was observed via transmission electron microscopy. Serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), IL-4, IL-5, IL-13, interferon-γ (IFN-γ) and tumor necrosis factor-α (TNF-α) levels were measured. Results Levels of IL-33 mRNA and protein did not change during ischemia (P >0.05) but increased significantly during reperfusion (P <0.05). After reperfusion for 6 hours, serum levels of ALT, AST, IL-4, IL-5, IL-13, IFN-γ and TNF-α were significantly increased (P <0.05), and hepatocellular ultrastructure was damaged. Pretreatment with IL-33 attenuated severity of liver damage compared with controls, but pretreatment with anti-ST2L antibody increased severity. Serum levels of IL-4, IL-5 and IL-13 protein increased whereas IFN-γ decreased following IL-33 pretreatment. Pretreatment with anti-ST2L antibody significantly decreased serum IL-4, IL-5, IL-13 levels and increased serum IFN-γ levels compared with controls (P <0.05). There was no change in the level of TNF-α. Conclusion IL-33 is produced systematically and locally in liver during I/R injury. Pretreatment with IL-33 is therapeutic for hepatic I/R injury, possibly via inducing a Th1 to Th2 shift.

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Zhu, Xiaoqing, Yinghua Zhao, Yuxue Jiang, Tianxue Qin, Jintong Chen, Xiao Chu, Qing Yi, Sujun Gao, and Siqing Wang. "Dectin-1 signaling inhibits osteoclastogenesis via IL-33-induced inhibition of NFATc1." Oncotarget 8, no. 32 (June 8, 2017): 53366–74. http://dx.doi.org/10.18632/oncotarget.18411.

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Travers, Jared, Mark Rochman, Cora E. Miracle, Jared P. Cohen, and Marc E. Rothenberg. "Linking impaired skin barrier function to esophageal allergic inflammation via IL-33." Journal of Allergy and Clinical Immunology 138, no. 5 (November 2016): 1381–83. http://dx.doi.org/10.1016/j.jaci.2016.09.001.

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Ono, Yosuke, Osamu Yoshino, Takehiro Hiraoka, Ikumi Akiyama, Erina Sato, Masami Ito, Mutsumi Kobayashi, et al. "IL-33 Exacerbates Endometriotic Lesions via Polarizing Peritoneal Macrophages to M2 Subtype." Reproductive Sciences 27, no. 3 (January 7, 2020): 869–76. http://dx.doi.org/10.1007/s43032-019-00090-9.

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Garth, Jaleesa M., Kristen M. Reeder, Matthew S. Godwin, Joseph J. Mackel, Chad W. Dunaway, Jonathan P. Blackburn, and Chad Steele. "IL-33 Signaling Regulates Innate IL-17A and IL-22 Production via Suppression of Prostaglandin E2 during Lung Fungal Infection." Journal of Immunology 199, no. 6 (August 7, 2017): 2140–48. http://dx.doi.org/10.4049/jimmunol.1602186.

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Howard, Chanie L., Donna C. Decker, Ivy Aneas Swanson, Kelly M. Blaine, Marcelo A. Nobrega, and Anne I. Sperling. "A novel role of human lung endothelial cells in allergic airway disease by producing and responding to IL-33." Journal of Immunology 200, no. 1_Supplement (May 1, 2018): 44.17. http://dx.doi.org/10.4049/jimmunol.200.supp.44.17.

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Abstract Allergic asthma affects more than 300 million people worldwide and is characterized by airway hypersensitivity and eosinophilia. A prevalent feature of allergic asthma is increased serum IL-33 levels, and asthma GWAS have demonstrated that SNPs in the IL-33 locus are significantly associated with disease. While IL-33 and its downstream type 2 responses have been extensively studied in murine models of asthma, much less is known about the regulation of human IL33. Analysis of the mouse and human IL33 loci reveals little genomic conservation between the two species in non-coding regions. We generated a novel BAC transgenic mouse strain containing the human IL-33 locus with a fluorescent reporter to interrogate the regulation and expression of human IL-33. Surprisingly, the mice expressed human IL-33 primarily in endothelial cells, whereas murine IL-33 was expressed primarily in epithelial cells. These results mirror the expression profiles of IL-33 in primary human lung cells from the LungGENS database, thus demonstrating that our novel mouse model faithfully replicates human IL-33 expression. To understand how human IL-33 in the lung is regulated and expressed during inflammation, we examined BAC transgenic mice challenged with either house dust mite extract (HDM) or poly(I:C). In contrast to murine IL-33, expression of human IL-33 was reduced during allergic inflammation. We tested whether IL-33 is able to autoregulate itself via a negative feedback loop. Indeed, IL-33 administration downregulated the expression of human IL-33 in lung endothelial cells. Together, these data emphasize a distinct and novel role in humans for lung endothelial cells in allergic airway disease by producing and responding to IL-33.

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Choi, Yeon-Sook, Hyun-Jung Choi, Jeong-Ki Min, Bo-Jeong Pyun, Yong-Sun Maeng, Hongryeol Park, Jihye Kim, Young-Myeong Kim, and Young-Guen Kwon. "Interleukin-33 induces angiogenesis and vascular permeability through ST2/TRAF6-mediated endothelial nitric oxide production." Blood 114, no. 14 (October 1, 2009): 3117–26. http://dx.doi.org/10.1182/blood-2009-02-203372.

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Interleukin-33 (IL-33), a member of the IL-1 cytokine family, is emerging as a new regulator of immune responses and inflammatory vascular diseases. Although IL-33 and its cognate receptor ST2 appear to be expressed in vascular cells, the precise role of IL-33 in the vasculature has not been determined. In this study, we report a novel role of IL-33 as a potent endothelial activator, promoting both angiogenesis and vascular permeability. IL-33 increased proliferation, migration, and morphologic differentiation of human endothelial cells, consistently with increased angiogenesis in vivo. IL-33 also increased endothelial permeability with reduced vascular endothelial–cadherin-facilitated cell–cell junctions in vitro and induced vascular leakage in mouse skin. These effects of IL-33 were blocked by knockdown of ST2. Ligation of IL-33 with ST2 rapidly increased endothelial nitric oxide (NO) production through TRAF6-mediated activation of phosphoinoside-3-kinase, Akt, and endothelial NO synthase. Moreover, pharmacologic or genetic blockage of endothelial NO generation resulted in the inhibition of angiogenesis and vascular hyperpermeability induced by IL-33. These data demonstrate that IL-33 promotes angiogenesis and vascular leakage by stimulating endothelial NO production via the ST2/TRAF6-Akt-eNOS signaling pathway. These findings open new perspectives for the role of IL-33 in the pathogenesis of angiogenesis-dependent and inflammatory vascular diseases.

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Matta, Benjamin, Jeremy Lott, Lisa Mathews, Brian Rosborough, Bruce Blazar, and Heth Turnquist. "IL-33 stimulates dendritic cell secretion of IL-2 that promotes selective expansion of ST2+Foxp3+ regulatory T cells (IRC5P.460)." Journal of Immunology 192, no. 1_Supplement (May 1, 2014): 125.9. http://dx.doi.org/10.4049/jimmunol.192.supp.125.9.

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Abstract IL-33 is a pleiotropic IL-1 family cytokine that signals via ST2 and expands ST2+Foxp3+ regulatory T cells (Treg) in vivo. As ST2+ Treg show poor expansion by direct IL-33 stimulation, we sought to define mechanisms mediating their expansion. IL-2 signaling promotes ST2 expression on CD4+ T cells, and dendritic cells (DC) express ST2 (able to respond to IL-33), and are a potential source of IL-2. Thus, we examined if IL-33 mediates ST2+ Treg expansion by stimulating DC IL-2 production. CD11c+ wild type (WT) or IL-2 knockout (KO) bone marrow DC were exposed to IL-33 or LPS. DC phenotype was evaluated by multi-color flow cytometric analysis. The influence of IL-33 DC on T cell function was evaluated in MLR with CD4+ T cells, and T cell proliferation and phenotype were determined by flow analysis. Cytokines were quantitated by ELISA. We found that unlike LPS, IL-33 does not influence DC surface phenotype or induce pro-inflammatory cytokine production compared to controls. However, IL-33 induces a 5-fold increase IL-2 production by DC. In MLR, IL-33 DC selectively expand an activated subset of ST2+Foxp3+ Treg that are CD44hiICOShi. IL-33 DC-derived IL-2 is critical since IL-33-exposed IL-2 KO DC fail to expand ST2+ Treg. In summary, IL-33 licenses DC to selectively expand a subset of activated Treg through production of IL-2, in the absence of classical DC activation. These findings may be harnessed to aid the development of novel therapeutics aimed at promoting immune tolerance.

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Journal articles on the topic 'Il-33 vih'

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