Group 2 innate lymphoid cell activation in the neonatal lung drives type 2 immunity and allergen sensitization

Steer, Catherine A.; Martínez-González, Itziar; Ghaedi, Maryam; Allinger, Patricia; Mathä, Laura; Takei, Fumio

doi:10.1016/j.jaci.2016.12.984

Cited by 70 publications

(123 citation statements)

References 11 publications

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“…28–30 Across the first two weeks, ILC2 rapidly accumulate in the lungs and reach levels comparable to adult mice. 28–31 This accumulation of ILC2 coincides with a wave of IL-33 expression in the lungs, primarily from nonhematopoietic (CD45 − ) Epithelial cell adhesion molecule expressing (EpCam + ) lung epithelial cells. 29 Conceptually, this IL-33 expression and ILC2 accumulation occurs during the alveolarization period of murine lung development with expansion and maturation of type II pneumocytes.…”

Section: Ilc Tissue Maintenance and Traffickingmentioning

confidence: 98%

“…Mice lacking IL-33 signaling had reduced numbers of ILC2 in the lungs at post-natal days 7, 10, and 14 consistent with a critical role for IL-33 in establishing the ILC2 compartment within the lungs. 28,29,31 In the lungs during the post-natal period, ILC2 are the major source of type 2 cytokines, and the recruitment of type 2-associated effector cells such as eosinophils and anti-inflammatory M2 macrophages critically depends upon ILC2. 29,31 Collectively, these changes promote type 2 immune skewing in the post-natal period that can be exacerbated with exposure to allergen and persist into adulthood.…”

Section: Ilc Tissue Maintenance and Traffickingmentioning

confidence: 99%

“…28,29,31 In the lungs during the post-natal period, ILC2 are the major source of type 2 cytokines, and the recruitment of type 2-associated effector cells such as eosinophils and anti-inflammatory M2 macrophages critically depends upon ILC2. 29,31 Collectively, these changes promote type 2 immune skewing in the post-natal period that can be exacerbated with exposure to allergen and persist into adulthood. While ILC2 accumulation has been well characterized in the lungs, substantially less is known about ILC2 accumulation in other tissues.…”

Section: Ilc Tissue Maintenance and Traffickingmentioning

confidence: 99%

See 2 more Smart Citations

Innate lymphoid cells and allergic disease

Stier

Peebles

2017

Annals of Allergy, Asthma & Immunology

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Section: Ilc Tissue Maintenance and Traffickingmentioning

confidence: 98%

Section: Ilc Tissue Maintenance and Traffickingmentioning

confidence: 99%

Section: Ilc Tissue Maintenance and Traffickingmentioning

confidence: 99%

See 1 more Smart Citation

Innate lymphoid cells and allergic disease

Stier

Peebles

2017

Annals of Allergy, Asthma & Immunology

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“…Despite the proposed importance of these effector cells in immune regulation and disease, and the intimate link with T‐helper cells, nothing is known about their role in immune maturation and early life development. Recent evidence indicates that the ILC2 population undergoes rapid expansion in the neonatal lung during the first few weeks of life …”

Section: Development Of Immunity In Early Lifementioning

confidence: 99%

“…Recent evidence indicates that the ILC2 population undergoes rapid expansion in the neonatal lung during the first few weeks of life. [107][108][109] Factors that may result in accentuated or prolonged Th2 skewing include maternal allergy 110 but environmental exposures are also critical as has become apparent from the farming exposure studies. 111 Growing up in close proximity to cows seems to provide protection and incidence of allergic diseases are greatly reduced in children who have grown up in farming communities.…”

Section: Innate Lymphoid Cells In Early Lifementioning

confidence: 99%

Development of allergic immunity in early life

Lloyd

Saglani

2017

Immunological Reviews

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The growth and maturity of the peripheral immune system and subsequent development of pulmonary immunity in early life is dictated by host, environmental and microbial factors. Dysregulation during the critical window of immune development in the postnatal years results in disease which impacts on lifelong lung health. Asthma is a common disease in childhood and is often preceded by wheezing illnesses during the preschool years. However, the mechanisms underlying development of wheeze and how and why only some children progress to asthma is unknown. Human studies to date have generally focused on peripheral immune development, with little assessment of local tissue pathology in young children. Moreover, mechanisms underlying the interactions between inflammation and tissue repair at mucosal surfaces in early life remain unknown. Disappointingly, mechanistic studies in mice have predominantly used adult models. This review will consider the aspects of the neonatal immune system which might contribute to the development of early life wheezing disorders and asthma, and discuss the external environmental factors which may influence this process.

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The immunological link between neonatal lung and eye disease

et al. 2021

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Bronchopulmonary dysplasia (BPD) and retinopathy of prematurity (ROP) are two neonatal diseases of major clinical importance, arising in large part as a consequence of supplemental oxygen therapy used to promote the survival of preterm infants. The presence of coincident inflammation in the lungs and eyes of neonates receiving oxygen therapy indicates that a dysregulated immune response serves as a potential common pathogenic factor for both diseases. This review examines the current state of knowledge of immunological dysregulation in BPD and ROP, identifying similarities in the cellular subsets and inflammatory cytokines that are found in the alveoli and retina during the active phase of these diseases, indicating possible mechanistic overlap. In addition, we highlight gaps in the understanding of whether these responses emerge independently in the lung and retina as a consequence of oxygen exposure or arise because of inflammatory spill‐over from the lung. As BPD and ROP are anatomically distinct, they are often considered discreet disease entities and are therefore treated separately. We propose that an improved understanding of the relationship between BPD and ROP is key to the identification of novel therapeutic targets to treat or prevent both conditions simultaneously.

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Group 2 innate lymphoid cell activation in the neonatal lung drives type 2 immunity and allergen sensitization

Cited by 70 publications

References 11 publications

Innate lymphoid cells and allergic disease

Innate lymphoid cells and allergic disease

Development of allergic immunity in early life

The immunological link between neonatal lung and eye disease

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