Direct platelet adhesion potentiates group 2 innate lymphoid cell functions

Orimo, Keisuke; Tamari, Masato; Takeda, Tomohiro; Kubo, Terufumi; Rückert, Beate; Motomura, Kenichiro; Sugiyama, Hiroki; Yamada, Ayako; Saito, Kyoko; Arae, Ken; Kuriyama, Motohiro; Hara, Mariko; Soyka, Michael; Ikutani, Masashi; Yamaguchi, Sota; Morimoto, Noriko; Nakabayashi, Kazuhiko; Hata, Kenichiro; Matsuda, Akio; Akdiş, Cezmi A.; Sudo, Katsuko; Saito, Hirohisa; Nakae, Susumu; Tamaoki, Jun; Tagaya, Etsuko; Matsumoto, Kenji; Morita, Hideaki

doi:10.1111/all.15057

Cited by 10 publications

(8 citation statements)

References 37 publications

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“…Further studies are needed to clarify the involvement of laundry-detergent residues contained in household dust in the development of asthma in the general population. IL-33, a key activator of ILC2s, 22,[66][67][68][69][70] is known to be constitutively expressed in the nuclei of endothelial and epithelial cells. [71][72][73][74][75] Its expression in airways is increased in patients with asthma [76][77][78] and allergic rhinitis.…”

Section: Discussionmentioning

confidence: 99%

Laundry detergents and surfactants‐induced eosinophilic airway inflammation by increasing IL‐33 expression and activating ILC2s

Saito

Orimo

Kubo

et al. 2023

Allergy

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Introduction Epidemiological studies demonstrated that cleaning work and frequent use of cleaning products are risk factors for asthma. Laundry detergents have been reported to have epithelial barrier‐opening effects. However, whether laundry detergents directly induce airway inflammation and its mechanisms in vivo remain to be elucidated. Methods Two commercial laundry detergents and two commonly used surfactants for cleaning and cosmetics (sodium lauryl sulfate and sodium dodecyl benzene sulfonate) were intranasally administered to mice. Lungs were analyzed using flow cytometry, histology, ELISA, and quantitative PCR. Human bronchial epithelial cells were stimulated with laundry detergents and analyzed using quantitative PCR and western blotting. Involvement of oxidative stress was assessed using an antioxidant. Dust samples from homes were analyzed to determine their detergent content by measuring their critical micelle concentration (CMC). Results The administered laundry detergents and surfactants‐induced eosinophilic airway inflammation accompanied by increased IL‐33 expression and activation of group 2 innate lymphoid cells (ILC2s). Detergent‐induced eosinophilic airway inflammation was significantly attenuated in Rag2−/−Il2rg−/−, Il33−/− mice, and also in wild‐type mice treated with NAC. Detergent‐induced IL‐33 expression in airways was attenuated by NAC treatment, both in vivo and in vitro. CMCs were found in all of the tested dust extracts, and they differed significantly among the homes. Conclusion The laundry detergents and surfactants‐induced eosinophilic airway inflammation in vivo through epithelial cell and ILC2 activation. They induced IL‐33 expression in airway epithelial cells through oxidative stress. Furthermore, detergent residues were present in house dust and are presumably inhaled into the airway in daily life.

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Section: Discussionmentioning

confidence: 99%

Laundry detergents and surfactants‐induced eosinophilic airway inflammation by increasing IL‐33 expression and activating ILC2s

Saito

Orimo

Kubo

et al. 2023

Allergy

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“…Myeloid dendritic cells (mDCs) from the nasal mucosa of AR patients can secrete IL‐33 to activate ILC2s via the IL‐33/ST2 pathway 5 . In the peripheral blood and airway mucosa of Alternaria ‐challenged mice, CD41 + platelets have been shown to spontaneously attach to ILC2s, and CD41 + ILC2s exhibit significantly higher proliferation and increased type 2 cytokine production in response to IL‐33 than CD41 − ILC2s 6 . However, how long it takes for platelets to fully potentiate ILC2s in the peripheral blood remains unknown.…”

Section: Pathomechanisms In Armentioning

confidence: 99%

“…5 In the peripheral blood and airway mucosa of Alternaria-challenged mice, CD41 + platelets have been shown to spontaneously attach to ILC2s, and CD41 + ILC2s exhibit significantly higher proliferation and increased type 2 cytokine production in response to IL-33 than CD41 − ILC2s. 6 However, how long it takes for platelets to fully potentiate ILC2s in the peripheral blood remains unknown. More recently, neuropeptides have been reported to be involved in ILC2 activation at mucosa sites.…”

Section: New Cognition Of Ilc2s In Armentioning

confidence: 99%

Update on pathomechanisms and treatments in allergic rhinitis

Zhang

Feng

Zhang

2022

Allergy

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Allergic rhinitis (AR) is a global health problem with increasing prevalence and association with an enormous medical and socioeconomic burden. New recognition of immune cells such as type 2 innate lymphocytes (ILC2s), T helper (Th2) 2 cells, follicular helper T cells, follicular regulatory T cells, regulatory T cells, B cells, dendritic cells, and epithelial cells in AR pathogenesis has been updated in this review paper. An in‐depth understanding of the mechanisms underlying AR will aid the identification of biomarkers associated with disease and ultimately provide valuable parameters critical to guide personalized targeted therapy. As the only etiological treatment option for AR, allergen‐specific immunotherapy (AIT) has attracted increasing attention, with evidence for effectiveness of AIT recently demonstrated in several randomized controlled trials and long‐term real‐life studies. The exploration of biologics as therapeutic options has only involved anti‐IgE and anti‐type 2 inflammatory agents; however, the cost‐effectiveness of these agents remains to be elucidated precisely. In the midst of the currently on‐going COVID‐19 pandemic, a global life‐threatening disease, although some studies have indicated that AR is not a risk factor for severity and mortality of COVID‐19, this needs to be confirmed in multi‐centre, real‐life studies of AR patients from different parts of the world.

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“…Platelets are versatile cells. They not only play pivotal roles in hemostasis and thrombosis, but also actively engage in other physio-/pathophysiological processes, e.g., immunity, inflammation, and atherosclerosis [ 1 – 7 ]. It is known that platelets are closely involved in regulation of CD4 + T cell immune responses [ 4 , 5 , 8 , 9 ].…”

Section: Introductionmentioning

confidence: 99%

Platelets fine-tune effector responses of naïve CD4+ T cells via platelet factor 4-regulated transforming growth factor β signaling

Hao

Liu

Tan

et al. 2022

Cell. Mol. Life Sci.

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Background and aim Platelets are an able regulator of CD4+ T cell immunity. Herein, the mechanisms underlying platelet-regulated effector responses of naïve CD4+ T (Tn) cells were investigated. Methods Platelet–Tn cell co-cultures of human cells, genetically modified murine models, and high-throughput bioinformatic analyses were combined to elucidate molecular mechanisms of platelet-dependent regulation. Results Platelets exerted sophisticated regulation on effector responses of type 1, 2, and 17 T helper (Th1/Th2/Th17) and regulatory T (Treg) cells, in time-, concentration-, and organ-dependent manners and with close cooperation of transforming growth factor β (TGFβ) and platelet factor 4 (PF4). PF4 at low concentrations reinforced TGFβ signaling by heteromerizing with type III TGFβ receptor (TGFBRIII), and subsequently enhanced TGFBRII expression and TGFβ signaling. High-concentration PF4 had, however, opposite effects by directly binding to TGFBRII, blocking TGFβ–TGFBRII ligation, and thus inhibiting TGFβ signaling. Furthermore, platelet depletion markedly hampered Treg and Th17 responses in the spleen but not in the lymph nodes, blockade of platelet–Tn cell contact diminished platelet effects, while spleen injection of PF4-immobilized microparticles in PF4-deficient mice mimicked platelet effects, suggesting the importance of direct platelet–Tn contact and platelet-bound PF4 for the optimal regulatory effects by platelets. Conclusion Platelets exert context-dependent regulations on effector responses of Tn cells via PF4-TGFβ duet, suggesting new possibilities of platelet-targeted interventions of T cell immunity.

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Direct platelet adhesion potentiates group 2 innate lymphoid cell functions

Cited by 10 publications

References 37 publications

Laundry detergents and surfactants‐induced eosinophilic airway inflammation by increasing IL‐33 expression and activating ILC2s

Laundry detergents and surfactants‐induced eosinophilic airway inflammation by increasing IL‐33 expression and activating ILC2s

Update on pathomechanisms and treatments in allergic rhinitis

Platelets fine-tune effector responses of naïve CD4+ T cells via platelet factor 4-regulated transforming growth factor β signaling

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