Basophils regulate the recruitment of eosinophils in a murine model of irritant contact dermatitis

Nakashima, Chisa; Otsuka, Atsushi; Kitoh, Akihiko; Honda, Tetsuya; Egawa, Gyohei; Nakajima, Saeko; Nakamizo, Satoshi; Arita, Makoto; Kubo, Masato

doi:10.1016/j.jaci.2014.02.026

Cited by 68 publications

(65 citation statements)

References 45 publications

(47 reference statements)

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Cross-linking of high affinity receptors with antigen-specific IgE complexes leads rapidly to degranulation and secretion of inflammatory mediators such as histamine, leukotrienes, cytokines and chemokines, which are important in the development of acute and chronic allergic responses [11,12]. In addition, a recent study suggests that basophils are able to infiltrate rapidly into the http inflamed skin and subsequently recruit eosinophils for the development of inflammatory lesions in murine models [13]. In that study, recruitment of eosinophils was induced by production of IL-4 and TNF-a from basophils in contact with fibroblasts, promoting the expression of eotaxin and RANTES from the fibroblasts.…”

Section: Introductionmentioning

confidence: 99%

House dust mite allergen Der f 1 induces IL-8 in human basophilic cells via ROS-ERK and p38 signal pathways

Kim

Jeong

et al. 2015

Cytokine

View full text Add to dashboard Cite

Section: Introductionmentioning

confidence: 99%

House dust mite allergen Der f 1 induces IL-8 in human basophilic cells via ROS-ERK and p38 signal pathways

Kim

Jeong

et al. 2015

Cytokine

View full text Add to dashboard Cite

“…However, recent studies have revealed that basophils and mast cells play distinct roles in immune responses such as allergic inflammation and protective immunity to parasitic infections (2)(3)(4). Basophils also contribute to immune regulation through their interaction with other types of cells, including T cells (5)(6)(7)(8), monocytes (9,10), innate lymphoid cells (11), fibroblasts (12,13), and endothelial cells (14).…”

mentioning

confidence: 99%

Trogocytosis of peptide–MHC class II complexes from dendritic cells confers antigen-presenting ability on basophils

Miyake

Shiozawa

Nagao

et al. 2017

Proc. Natl. Acad. Sci. U.S.A.

108

101

View full text Add to dashboard Cite

Th2 immunity plays important roles in both protective and allergic responses. Nevertheless, the nature of antigen-presenting cells responsible for Th2 cell differentiation remains ill-defined compared with the nature of the cells responsible for Th1 and Th17 cell differentiation. Basophils have attracted attention as a producer of Th2-inducing cytokine IL-4, whereas their MHC class II (MHC-II) expression and function as antigen-presenting cells are matters of considerable controversy. Here we revisited the MHC-II expression on basophils and explored its functional relevance in Th2 cell differentiation. Basophils generated in vitro from bone marrow cells in culture with IL-3 plus GM-CSF displayed MHC-II on the cell surface, whereas those generated in culture with IL-3 alone did not. Of note, these MHC-II–expressing basophils showed little or no transcription of the corresponding MHC-II gene. The GM-CSF addition to culture expanded dendritic cells (DCs) other than basophils. Coculture of basophils and DCs revealed that basophils acquired peptide–MHC-II complexes from DCs via cell contact-dependent trogocytosis. The acquired complexes, together with CD86, enabled basophils to stimulate peptide-specific T cells, leading to their proliferation and IL-4 production, indicating that basophils can function as antigen-presenting cells for Th2 cell differentiation. Transfer of MHC-II from DCs to basophils was also detected in draining lymph nodes of mice with atopic dermatitis-like skin inflammation. Thus, the present study defined the mechanism by which basophils display MHC-II on the cell surface and appears to reconcile some discrepancies observed in previous studies.

show abstract

“…39 Co-cultivation with fibroblasts increased basophil CCL5 expression, while basophils induced elevated eotaxin/CCL11 expression in the fibroblasts. 39 In our results, a large number of dermal fibroblasts and a dramatic infiltration of basophils and eosinophils were observed in the AD-like skin lesions (Figure 3). Because they are accessible to each other in vivo, we hypothesized that basophils and eosinophils might be activated in synergy with dermal fibroblasts in response to NOD2/TLR2 ligands.…”

Section: Discussionmentioning

confidence: 93%

NOD2 and TLR2 ligands trigger the activation of basophils and eosinophils by interacting with dermal fibroblasts in atopic dermatitis-like skin inflammation

et al. 2015

View full text Add to dashboard Cite

The skin of patients with atopic dermatitis (AD) has a unique predisposition for colonization by Staphylococcus aureus (S. aureus), which contributes to the inflammation and grim prognosis of AD. Although the mechanism underlying the S. aureus-induced exacerbation of AD remains unclear, recent studies have found a pivotal role for pattern recognition receptors in regulating the inflammatory responses in S. aureus infection. In the present study, we used a typical mouse model of AD-like skin inflammation and found that S. aureus-associated nucleotide-binding oligomerization domain-containing protein 2 (NOD2) and toll-like receptor 2 (TLR2) ligands exacerbated AD-like symptoms, which were further deteriorated by the in vivo expansion of basophils and eosinophils. Subsequent histological analyses revealed that dermal fibroblasts were pervasive in the AD-like skin lesions. Co-culture of human dermal fibroblasts with basophils and eosinophils resulted in a vigorous cytokine/chemokine response to the NOD2/TLR2 ligands and the enhanced expression of intercellular adhesion molecule-1 on the dermal fibroblasts. Basophils and eosinophils were primarily responsible for the AD-related cytokine/chemokine expression in the co-cultures. Direct intercellular contact was necessary for the crosstalk between basophils and dermal fibroblasts, while soluble mediators were sufficient to mediate the eosinophil-fibroblast interactions. Moreover, the intracellular p38 mitogen-activated protein kinase, extracellular signal-regulated kinase, and nuclear factor-kappa B signaling pathways were essential for NOD2/TLR2 ligand-mediated activation of basophils, eosinophils, and dermal fibroblasts in AD-related inflammation. This study provides the evidence of NOD2/TLR2-mediated exacerbation of AD through activation of innate immune cells and therefore sheds light on a novel mechanistic pathway by which S. aureus contributes to the pathophysiology of AD. Cellular & Molecular Immunology

show abstract

Basophils regulate the recruitment of eosinophils in a murine model of irritant contact dermatitis

Cited by 68 publications

References 45 publications

House dust mite allergen Der f 1 induces IL-8 in human basophilic cells via ROS-ERK and p38 signal pathways

House dust mite allergen Der f 1 induces IL-8 in human basophilic cells via ROS-ERK and p38 signal pathways

Trogocytosis of peptide–MHC class II complexes from dendritic cells confers antigen-presenting ability on basophils

NOD2 and TLR2 ligands trigger the activation of basophils and eosinophils by interacting with dermal fibroblasts in atopic dermatitis-like skin inflammation

Contact Info

Product

Resources

About