Innate Lymphoid Cells in Type 2 Immune Responses

Mirchandani, Ananda S.; Salmond, Robert J.

doi:10.1007/s00005-014-0327-5

Cited by 3 publications

(3 citation statements)

References 61 publications

(90 reference statements)

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“…Characteristic surface markers and receptors for chemokines, which are involved in the distribution of lymphoid cells to specific organ sites, are expressed by ILC2s [11]. Two transcription factors, RORα and GATA3, which are stimulated by IL-7, are required for the development of ILC2s [12]. Upon stimulation with Th2 polarizing cytokines such as IL-25, IL-33, and thymic stromal lymphopoietin (TSLP), mature ILC2s start to produce Th2 cell type cytokines that participate in the progression of allergic asthma [13].…”

Section: Introductionmentioning

confidence: 99%

miR-146a Mimics Attenuate Allergic Airway Inflammation by Impacted Group 2 Innate Lymphoid Cells in an Ovalbumin-Induced Asthma Mouse Model

Han¹,

Ma²,

Bao³

et al. 2018

Int Arch Allergy Immunol

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Background: The prevalence of allergic asthma has increased dramatically. Previous studies have found that the microRNA 146a (miR-146a) expression in asthma inhibits cell proliferation and promotes apoptosis of bronchial smooth muscle cells. We aimed to investigate the effect of miR-146a mimics on ovalbumin (OVA)-induced asthma in a mouse model. Methods: Inflammatory cell infiltration in bronchoalveolar lavage fluid (BALF) was measured by flow cytometry. Levels of OVA-specific immunoglobulin E (IgE) in serum and cytokines in BALF were examined by enzyme-linked immunosorbent assay. For monitoring the airway, the Penh value (% baseline) was measured using a whole-body plethysmograph. Results: In OVA-induced asthmatic mice, miR-146a significantly suppressed the infiltration of inflammatory cells in BALF and decreased the levels of OVA-specific IgE and T helper 2 cell type cytokines. In addition, miR-146a inhibited the OVA-induced airway hyperresponsiveness and the group 2 innate lymphoid cell responses. Moreover, the effects of miR-146a mimics were dependent on interleukin 33 stimulation. Conclusions: Our results suggest that miR-146a mimics might serve as an attractive candidate for further preclinical studies as an anti-inflammatory treatment of asthma.

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Section: Introductionmentioning

confidence: 99%

miR-146a Mimics Attenuate Allergic Airway Inflammation by Impacted Group 2 Innate Lymphoid Cells in an Ovalbumin-Induced Asthma Mouse Model

Han¹,

Ma²,

Bao³

et al. 2018

Int Arch Allergy Immunol

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“…IL-5 is expressed by Th2-cells [14], eosinophils [63], basophils [64], innate lymphoid type 2 cells (ILC2) and iNKT-cells [65,66]. Its level is increased in the oesophagus of EoE patients [67].…”

Section: Putting the Puzzle Togethermentioning

confidence: 99%

Allergic mechanisms of Eosinophilic oesophagitis

Leung¹,

Beukema²,

Shen³

2015

Best Practice & Research Clinical Gastroenterology

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Eosinophilic oesophagitis (EoE) is characterized by oesophageal dysfunction and oesophageal eosinophilia refractory to proton-pump-inhibitor treatment. EoE is a food allergy, as elimination of food trigger(s) abrogates the disease, while trigger(s) reintroduction causes recurrence. The allergic mechanism of EoE involves both IgE and non-IgE processes. There is a break in oral tolerance, the immune mechanism allowing enteric exposure to food and micro-organisms without causing deleterious immune responses. Changes in life-style, alterations in gut flora and use of antibiotics may be increasing disease prevalence. Mouse models of EoE and human studies revealed the role of regulatory T-cells and iNKT-cells in the pathogenesis. Th2-cytokines like IL-4, IL-5 and IL-13, and other cytokines like TGFβ and TSLP are involved. Perhaps no one cytokine is critically important for driving the disease. Control of EoE may require a pharmaceutical approach that blocks more than one target in the Th2-inflammatory pathway.

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“…Like other galectins, gal-3 is abundantly expressed at the fetal maternal interface, showing a localization pattern that partially overlaps that of gal-1 [24,41]. The interplay between these lectins may be important for fine-tuning the maternal immune response during early pregnancy, as gal-3 is mainly considered a pro-inflammatory signal promoting the activation, degranulation and cytokine secretion of diverse innate immune cell subsets [42,43]. Gal-3 can also promote T cell proliferation and activation [42,44], whereas its effect on T cell survival can be either stimulatory or inhibitory depending on its association with intracellular or extracellular targets [18,45].…”

Section: Galectin-3mentioning

confidence: 99%

A potential pathophysiological role for galectins and the renin–angiotensin system in preeclampsia

Blois

Dechend

Barrientos

et al. 2014

Cell. Mol. Life Sci.

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This review discusses a potential role of galectins and the renin-angiotensin system (RAS) in the pathophysiology of preeclampsia (PE). Preeclampsia affects between 3 and 5 % of all pregnancies and is a heterogeneous disease, which may be caused by multiple factors. The only cure is the delivery of the placenta, which may result in a premature delivery and baby. Probably due to its heterogeneity, PE studies in human have hitherto only led to the identification of a limited number of factors involved in the pathogenesis of the disease. Animal models, particularly in mice and rats, have been used to gain further insight into the molecular pathology behind PE. In this review, we discuss the picture emerging from human and animal studies pointing to galectins and the RAS being associated with the PE syndrome and affecting a broad range of cellular signaling components. Moreover, we review the epidemiological evidence for PE increasing the risk of future cardiovascular disease later in life.

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Innate Lymphoid Cells in Type 2 Immune Responses

Cited by 3 publications

References 61 publications

miR-146a Mimics Attenuate Allergic Airway Inflammation by Impacted Group 2 Innate Lymphoid Cells in an Ovalbumin-Induced Asthma Mouse Model

miR-146a Mimics Attenuate Allergic Airway Inflammation by Impacted Group 2 Innate Lymphoid Cells in an Ovalbumin-Induced Asthma Mouse Model

Allergic mechanisms of Eosinophilic oesophagitis

A potential pathophysiological role for galectins and the renin–angiotensin system in preeclampsia

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