Circulating activated innate lymphoid cells and mucosal-associated invariant T cells are associated with airflow limitation in patients with asthma

Ishimori, A; Harada, Norihiro; Chiba, Asako; Harada, Sonoko; Matsuno, Kei; Makino, Fumihiko; Ito, Jun; Ono, Junya; Atsuta, Ryo; Izuhara, Kenji; Takahashi, Kazuhisa; Miyake, Sachiko

doi:10.1016/j.alit.2016.07.005

Cited by 24 publications

(16 citation statements)

References 48 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…40,41 Furthermore, increased numbers of ILC2s and higher IL-33 levels in BAL fluid were significantly associated with poor lung function in asthmatics. [42][43][44] There have also been reports that asthma severity and control levels are associated with the numbers of ILC2s. 41,45 Patients with severe asthma had significantly higher numbers of ILC2s in blood and sputum than patients with mild asthma, 41 and patients with uncontrolled or only partly controlled asthma also had significantly higher numbers of ILC2s than patients with well-controlled asthma and healthy controls.…”

Section: Discussionmentioning

confidence: 99%

Aggravation of asthmatic inflammation by chlorine exposure via innate lymphoid cells and CD11c^intermediate macrophages

Shim

Lee

Park

et al. 2019

Allergy

View full text Add to dashboard Cite

Background Chlorine is widely used in daily life as disinfectant. However, chronic exposure to chlorine products aggravates allergic TH2 inflammation and airway hyperresponsiveness (AHR). Innate lymphoid cells (ILCs) in airways contribute to the inception of asthma in association with virus infection, pollution, and excess of nutrient, but it is not known whether chronic chlorine exposure can activate innate immune cells. The aim of this study was to evaluate the impact of chlorine inhalation on the innate immunity such as ILCs and macrophages in relation with the development of asthma by using murine ovalbumin (OVA) sensitization/challenge model. Methods Six‐week‐old female BALB/c mice were sensitized and challenged with OVA in the presence and absence of chronic low‐dose chlorine exposure by inhalation of naturally vaporized gas of 5% sodium hypochlorite solution. AHR, airway inflammatory cells, from BALF and the population of ILCs and macrophages in the lung were evaluated. Results The mice exposed to chlorine with OVA (Cl + OVA group) showed enhanced AHR and eosinophilic inflammation compared to OVA‐treated mice (OVA group). The population of TH2 cells, ILC2s, and ILC3s increased in Cl + OVA group compared with OVA group. CD11cint macrophages also remarkably increased in Cl + OVA group compared with OVA group. The deletion of macrophages by clodronate resulted in reduction of ILC2s and ILC3s population which was restored by adoptive transfer of CD11cint macrophages. Conclusions Chronic chlorine inhalation contributes to the exacerbation of airway inflammation in asthmatic airway by mobilizing pro‐inflammatory macrophage into the lung as well as stimulating group 2 and 3 ILCs.

show abstract

Section: Discussionmentioning

confidence: 99%

Aggravation of asthmatic inflammation by chlorine exposure via innate lymphoid cells and CD11c^intermediate macrophages

Shim

Lee

Park

et al. 2019

Allergy

View full text Add to dashboard Cite

show abstract

“…The reduced MAIT cell frequency in blood was more pronounced in moderate-to-severe-COPD patients, and it was associated with elevated serum C-reactive protein levels and a reduced lung function [118]. Consistent with a role of ICS in modulating MAIT cell numbers, these were also found to be significantly reduced in the blood and lung tissue of ICS-treated asthma patients relative to normal individuals [119, 120], a result that was especially prominent in patients with severe asthma [120]. Together, these studies suggest that MAIT cells are susceptible to ICS treatment and that their deficiency may be associated with a more severe respiratory pathology.…”

Section: Mucosal-associated Invariant T Cellsmentioning

confidence: 99%

Innate Immunity of the Lung: From Basic Mechanisms to Translational Medicine

et al. 2018

View full text Add to dashboard Cite

The respiratory tract is faced daily with 10,000 L of inhaled air. While the majority of air contains harmless environmental components, the pulmonary immune system also has to cope with harmful microbial or sterile threats and react rapidly to protect the host at this intimate barrier zone. The airways are endowed with a broad armamentarium of cellular and humoral host defense mechanisms, most of which belong to the innate arm of the immune system. The complex interplay between resident and infiltrating immune cells and secreted innate immune proteins shapes the outcome of host-pathogen, host-allergen, and host-particle interactions within the mucosal airway compartment. Here, we summarize and discuss recent findings on pulmonary innate immunity and highlight key pathways relevant for biomarker and therapeutic targeting strategies for acute and chronic diseases of the respiratory tract.

show abstract

“…It is important to note that the classification scheme remains somewhat fluid and grouping is not absolute, as NK cells and ILC1 do not always require T-bet ( 9 ), and ILC2 and ILC3 can both convert to ILC1 ( 10 ), underscoring the inherent plasticity of these cell types. To further complicate matters, innate subsets of lymphoid cells may also include mucosal-associated invariant T cells ( 11 ), which express a semi-invariant T cell receptor and defined phenotypically as CD3 + Vα7.2 TCR + CD161 high cells in humans ( 12 , 13 ). In addition to their cellular and functional plasticity, ILC have a wide tissue distribution and thus are thought to be some of the earliest responders to infections and other inflammatory stimuli, but the full mechanisms involved are still poorly understood.…”

Section: Introductionmentioning

confidence: 99%

Innate Lymphoid Cells in HIV/SIV Infections

et al. 2017

View full text Add to dashboard Cite

Over the past several years, new populations of innate lymphocytes have been described in mice and primates that are critical for mucosal homeostasis, microbial regulation, and immune defense. Generally conserved from mice to humans, innate lymphoid cells (ILC) have been divided primarily into three subpopulations based on phenotypic and functional repertoires: ILC1 bear similarities to natural killer cells; ILC2 have overlapping functions with TH2 cells; and ILC3 that share many functions with TH17/TH22 cells. ILC are specifically enriched at mucosal surfaces and are possibly one of the earliest responders during viral infections besides being involved in the homeostasis of gut-associated lymphoid tissue and maintenance of gut epithelial barrier integrity. Burgeoning evidence also suggests that there is an early and sustained abrogation of ILC function and numbers during HIV and pathogenic SIV infections, most notably ILC3 in the gastrointestinal tract, which leads to disruption of the mucosal barrier and dysregulation of the local immune system. A better understanding of the direct or indirect mechanisms of loss and dysfunction will be critical to immunotherapeutics aimed at restoring these cells. Herein, we review the current literature on ILC with a particular emphasis on ILC3 and their role(s) in mucosal immunology and the significance of disrupting the ILC niche during HIV and SIV infections.

show abstract

Circulating activated innate lymphoid cells and mucosal-associated invariant T cells are associated with airflow limitation in patients with asthma

Abstract: For the first time, our data showed that activated NK cells, ILC1s, ILC2s, ILC3s, and MAIT cells were positively correlated with each other and may be associated with airflow limitation in patients with asthma.

Cited by 24 publications

References 48 publications

Aggravation of asthmatic inflammation by chlorine exposure via innate lymphoid cells and CD11c^intermediate macrophages

Aggravation of asthmatic inflammation by chlorine exposure via innate lymphoid cells and CD11c^intermediate macrophages

Innate Immunity of the Lung: From Basic Mechanisms to Translational Medicine

Innate Lymphoid Cells in HIV/SIV Infections

Contact Info

Product

Resources

About

Circulating activated innate lymphoid cells and mucosal-associated invariant T cells are associated with airflow limitation in patients with asthma

Abstract: For the first time, our data showed that activated NK cells, ILC1s, ILC2s, ILC3s, and MAIT cells were positively correlated with each other and may be associated with airflow limitation in patients with asthma.

Cited by 24 publications

References 48 publications

Aggravation of asthmatic inflammation by chlorine exposure via innate lymphoid cells and CD11cintermediate macrophages

Aggravation of asthmatic inflammation by chlorine exposure via innate lymphoid cells and CD11cintermediate macrophages

Innate Immunity of the Lung: From Basic Mechanisms to Translational Medicine

Innate Lymphoid Cells in HIV/SIV Infections

Contact Info

Product

Resources

About

Aggravation of asthmatic inflammation by chlorine exposure via innate lymphoid cells and CD11c^intermediate macrophages

Aggravation of asthmatic inflammation by chlorine exposure via innate lymphoid cells and CD11c^intermediate macrophages