The role of IL-33/ST2L signals in the immune cells

Lü, Jingli; Kang, Jian; Zhang, Chengliang; Zhang, Xiaojian

doi:10.1016/j.imlet.2015.01.008

Cited by 64 publications

(66 citation statements)

References 96 publications

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“…A variety of cytokine-producing cells respond to IL-33. This list continues to grow and currently includes mast cells, basophils, eosinophils, ILC2, some TH2 cells, and macrophages (54–58). Therefore our results demonstrate that LA can antagonize IL-33-induced systemic cytokine production in vivo, but do not restrict these effects to a specific lineage.…”

Section: Discussionmentioning

confidence: 99%

Lactic Acid Suppresses IL-33–Mediated Mast Cell Inflammatory Responses via Hypoxia-Inducible Factor-1α–Dependent miR-155 Suppression

Abebayehu

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Qayum

et al. 2016

The Journal of Immunology

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Lactic acid (LA) is present in tumors, asthma, and wound healing, environments with elevated IL-33 and mast cell infiltration. While IL-33 is a potent mast cell activator, how LA affects IL-33-mediated mast cell function is unknown. To investigate this, mouse bone marrow-derived mast cells (BMMC) were cultured with or without LA and activated with IL-33. LA reduced IL-33-mediated cytokine and chemokine production. Using inhibitors for monocarboxylate transporters (MCT) or replacing LA with sodium lactate revealed that LA effects are MCT-1- and pH-dependent. LA selectively altered IL-33 signaling, suppressing TAK1, JNK, ERK, and NFκB phosphorylation, but not p38 phosphorylation. LA effects in other contexts have been linked to HIF-1α, which was enhanced in BMMC treated with LA. Since HIF-1α has been shown to regulate the microRNA miR-155 in other systems, LA effects on miR-155-5p and -3p species were measured. In fact, LA selectively suppressed miR-155-5p in a HIF-1α-dependent manner. Moreover, overexpressing miR-155-5p, but not miR-155-3p, abolished LA effects on IL-33-induced cytokine production. These in vitro effects of reducing cytokines were consistent in vivo, since LA injected intraperitoneally into C57BL/6 mice suppressed IL-33-induced plasma cytokine levels. Lastly, IL-33 effects on primary human mast cells were suppressed by LA in an MCT-dependent manner. Our data demonstrate that LA, present in inflammatory and malignant microenvironments, can alter mast cell behavior to suppress inflammation.

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Section: Discussionmentioning

confidence: 99%

Lactic Acid Suppresses IL-33–Mediated Mast Cell Inflammatory Responses via Hypoxia-Inducible Factor-1α–Dependent miR-155 Suppression

Abebayehu

Spence

Qayum

et al. 2016

The Journal of Immunology

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“…Both molecules were originally shown to modulate innate immunity, however later, a role in the regulation of the adaptive immune response became apparent. For example, RA and IL-33 are molecules released during the initiation of inflammation, and their effect can impact the biology of several leukocyte lineages, including macrophages, basophils, NK cells, neutrophils, among others [9][10][11]. In general terms, both RA and IL-33 function as mediators of inflammation with enhancing or amplification roles.…”

Section: Discussionmentioning

confidence: 99%

IL-33 enhances retinoic acid signaling on CD4+ T cells

et al. 2016

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“…After antipsychotic treatment significant decrease of IL-13 was observed, suggesting that the BNDF-IL-13 interaction could be more thoroughly explored in schizophrenia (77). Also, IL-33, recently discovered IL-1 family member, plays a role in induction of airway contraction by stimulating expansion of IL-13-producing innate lymphoid cells (78). IL-33/ST2 signalling pathway regulates Т cells, differentiation and activation of dendritic cells, activation of macrophages and mast cells and production of type 2 cytokine producing innate lymphoid cells, showed to be important in type-2 immune response in development of spontaneous obesity (79) and atopic disorders, particularly asthma (80).…”

Section: Bdnf and Cytokines In Schizophrenia And Atopic Diseasesmentioning

confidence: 99%