The Metabolic Requirements of Th2 Cell Differentiation

Stark, Julian M.; Tibbitt, Christopher A.; Coquet, Jonathan M.

doi:10.3389/fimmu.2019.02318

Cited by 114 publications

(114 citation statements)

References 151 publications

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“…In addition to granulocyte adhesion, a number of these cytokines are involved in the recruitment of mononuclear leukocytes, a key step in the initiation and progression of inflammation. IPA also suggested differentiation of T H 2 cells, which are known to play an important role in mediating the inflammatory response 34 . T H 2 cells induce the recruitment of eosinophils, which could further explain the increased eosinophils in lewisite‐exposed animals.…”

Section: Discussionmentioning

confidence: 93%

“…IPA also suggested differentiation of T H 2 cells, which are known to play an important role in mediating the inflammatory response. 34 T H 2 cells induce the recruitment of eosinophils, which could further explain the increased eosinophils in lewisite-exposed animals. Consistent with increased neutrophils, MPO, a marker for neutrophil activation, was also significantly increased in lung tissues.…”

Section: Discussionmentioning

confidence: 96%

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Cutaneous lewisite exposure causes acute lung injury

Manzoor

Mariappan

Zafar

et al. 2020

Annals of the New York Academy of Sciences

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Lewisite is a strong vesicating and chemical warfare agent. Because of the rapid transdermal absorption, cutaneous exposure to lewisite can also elicit severe systemic injury. Lewisite (2.5, 5.0, and 7.5 mg/kg) was applied to the skin of Ptch1 +/− /SKH-1 mice and acute lung injury (ALI) was assessed after 24 hours. Arterial blood gas measurements showed hypercapnia and hypoxemia in the lewisite-exposed group. Histological evaluation of lung tissue revealed increased levels of proinflammatory neutrophils and a dose-dependent increase in structural changes indicative of injury. Increased inflammation was also confirmed by altered expression of cytokines, including increased IL-33, and a dose-dependent elevation of CXCL1, CXCL5, and GCSF was observed in the lung tissue. In the bronchoalveolar lavage fluid of lewisite-exposed animals, there was a significant increase in HMGB1, a damage-associated molecular pattern molecule, as well as elevated CXCL1 and CXCL5, which coincided with an influx of neutrophils to the lungs. Complete blood cell analysis revealed eosinophilia and altered neutrophil-lymphocyte ratios as a consequence of lewisite exposure. Mean platelet volume and RBC distribution width, which are predictors of lung injury, were also increased in the lewisite group. These data demonstrate that cutaneous lewisite exposure causes ALI and may contribute to mortality in exposed populations.

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Section: Discussionmentioning

confidence: 93%

Section: Discussionmentioning

confidence: 96%

Cutaneous lewisite exposure causes acute lung injury

Manzoor

Mariappan

Zafar

et al. 2020

Annals of the New York Academy of Sciences

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“…The kinase mTOR intervene in T helper growth, proliferation, and metabolism. Th1, Th2, and Th17 differentiation depends on mTOR activity while its inhibition favors Treg differentiation [39,40]. mTORc1 activation is required for differentiation towards all effectors lineages including Th2, since its inhibition through RAPTOR deletion powerfully interrupt the process and induces Th17 differentiation [41,42].…”

Section: Hormones Chromosomes Immunity and Allergymentioning

confidence: 99%

“…The downstream target of mTORc2 serine/threonine-protein kinase (SGK1) blocks Th1 cell lineage commitment and and promotes Th2 development. Furthermore deletion of another target of mTORc2 the GTPase RhoA reduces glycolisis and IL-4 secretion and Th1, Th2 and Th17 growth and fuction is highly glycolytic [39,44]. To enhance Tregs generation in normally activated conditions, the simultaneous inhibition of mTORC1 and mTORc2 [41,45] is required.…”

Section: Hormones Chromosomes Immunity and Allergymentioning

confidence: 99%

Sex and Gender Aspects for Patient Stratification in Allergy Prevention and Treatment

Martinis

Sirufo

Suppa

et al. 2020

IJMS

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Allergies are rapidly worsening in recent decades, representing the most common immunological diseases. The mechanism of disorders such as asthma, rhinocongiuntivitis, urticaria, atopic dermatitis, food and drug allergies, and anaphylaxis still remain unclear and consequently treatments is mostly still symptomatic and aspecific while developments of new therapies are limited. A growing amount of data in the literature shows us how the prevalence of allergic diseases is different in both sexes and its changes over the course of life. Genes, hormones, environmental and immunological factors affect sex disparities associated with the development and control of allergic diseases, while they more rarely are considered and reported regarding their differences related to social, psychological, cultural, economic, and employment aspects. This review describes the available knowledge on the role of sex and gender in allergies in an attempt to improve the indispensable gender perspective whose potential is still underestimated while it represents a significant turning point in research and the clinic. It will offer insights to stimulate exploration of the many aspects still unknown in this relationship that could ameliorate the preventive, diagnostic, and therapeutic strategies in allergic diseases.

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“…The skin barrier function repair remains the mainstay in the management of AD. Type2 T helper (Th2) cells are considered to play an essential role in the immune abnormalities of AD 6 , 7 . Interleukin (IL)-13, a Th2 cytokine, is suggested to suppress the expression of filaggrin (FLG), loricrin (LOR), and involucrin (IVL) in keratinocytes 4 , 8 , which are important proteins for skin barrier structure.…”

Section: Introductionmentioning

confidence: 99%

Rapamycin blocks the IL-13-induced deficiency of Epidermal Barrier Related Proteins via upregulation of miR-143 in HaCaT Keratinocytes

Jia

2020

Int. J. Med. Sci.

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Interleukin (IL)-13 plays a key role in the pathogenesis of atopic dermatitis (AD). Our preliminary study demonstrated that forced expression of miR-143 could block IL-13-induced down-regulation of epidermal barrier related proteins in epidermal keratinocytes. As previous studies suggested that miR-143 expression was regulated by mammalian target of rapamycin (mTOR) signaling pathway, we investigated the mechanism of mTOR signaling pathway in the epidermal barrier dysfunction of AD. The HaCaT cells were stimulated by IL-13 and subsequently treated with rapamycin. The expression levels of miR-143, IL-13 receptor α1 (IL-13Rα1), p-mTOR, p-S6K1, p-Akt, and epidermal barrier related proteins were analyzed through RT-qPCR and/or western blotting. The current study showed that IL-13 increased the expression levels of p-mTOR, p-S6K1, and p-Akt, and that rapamycin blocked IL-13-induced down-regulation of miR-143, suppressed the IL-13Rα1 expression and up-regulated the expressions of filaggrin, loricrin, and involucrin in HaCaT cells. This study proposed that IL-13 could activate the mTOR signaling pathway, and confirmed the vital role of mTOR-miR-143 signaling axis in the pathogenesis of AD. It provided solid evidences regarding rapamycin as a potential effective therapeutic option in the management of AD.

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The Metabolic Requirements of Th2 Cell Differentiation

Cited by 114 publications

References 151 publications

Cutaneous lewisite exposure causes acute lung injury

Cutaneous lewisite exposure causes acute lung injury

Sex and Gender Aspects for Patient Stratification in Allergy Prevention and Treatment

Rapamycin blocks the IL-13-induced deficiency of Epidermal Barrier Related Proteins via upregulation of miR-143 in HaCaT Keratinocytes

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