Evidence for a differential expression of the FcεRIγ chain in dendritic cells of atopic and nonatopic donors

Novak, Natalija; Tepel, Carmen; Koch, Susanne; Brix, Klaudia; Bieber, Thomas; Kraft, Stefan

doi:10.1172/jci15932

Cited by 69 publications

(76 citation statements)

References 45 publications

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“…We also acknowledge that the present findings do not preclude parallel contributions from activated invariant NKT cells, which have been suggested to contribute to lung AAM programming/activation in both human (50) and experimental asthma (16). Indeed, we have observed up-regulation of expression of the invariant NKT activation protein CD1d in the exacerbation-associated samples (not shown), but have not detected consistent exacerbation-associated changes in the circulating invariant NKT population.…”

Section: Discussioncontrasting

confidence: 43%

“…As noted in Fig. 3, type 1 IFN exposure in vitro can reproduce the FcRI␥ component of the asthma exacerbation-associated expression signature, which in other settings has been associated with indirect enhancement of surface expression of FcRI␣ protein on human and murine DC (50,51). However, as shown in Fig.…”

Section: Discussionmentioning

confidence: 89%

“…2, A-E) during acute exacerbations, with concomitant up-regulation of the gene encoding the FcRI␥-chain (Table II), which stabilizes the FcRI␣-chain on the cell surface (50). This infers transmission from the infected airway mucosa of an activation signal to monocytes/DC in the blood and/or bone marrow.…”

Section: Discussionmentioning

confidence: 99%

See 2 more Smart Citations

Interactions between Innate Antiviral and Atopic Immunoinflammatory Pathways Precipitate and Sustain Asthma Exacerbations in Children

Subrata

Bizzintino

Mamessier

et al. 2009

The Journal of Immunology

188

172

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Severe asthma exacerbations in children requiring hospitalization are typically associated with viral infection and occur almost exclusively among atopics, but the significance of these comorbidities is unknown. We hypothesized that underlying interactions between immunoinflammatory pathways related to responses to aeroallergen and virus are involved, and that evidence of these interactions is detectable in circulating cells during exacerbations. To address this hypothesis we used a genomics-based approach involving profiling of PBMC subpopulations collected during exacerbation vs convalescence by microarray and flow cytometry. We demonstrate that circulating T cells manifest the postactivated “exhausted” phenotype during exacerbations, whereas monocyte/dendritic cell populations display up-regulated CCR2 expression accompanied by phenotypic changes that have strong potential for enhancing local inflammation after their recruitment to the atopic lung. Notably, up-regulation of FcεR1, which is known to markedly amplify capacity for allergen uptake/presentation to Th2 effector cells via IgE-mediated allergen capture, and secondarily programming of IL-4/IL-13-dependent IL-13R+ alternatively activated macrophages that have been demonstrated in experimental settings to be a potent source of autocrine IL-13 production. We additionally show that this disease-associated activation profile can be reproduced in vitro by cytokine exposure of atopic monocytes, and furthermore that IFN-α can exert both positive and negative roles in the process. Our findings suggest that respiratory viral infection in atopic children may initiate an atopy-dependent cascade that amplifies and sustains airway inflammation initiated by innate antiviral immunity via harnessing underlying atopy-associated mechanisms. These interactions may account for the unique susceptibility of atopics to severe viral-induced asthma exacerbations.

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Section: Discussioncontrasting

confidence: 43%

Section: Discussionmentioning

confidence: 89%

See 1 more Smart Citation

Interactions between Innate Antiviral and Atopic Immunoinflammatory Pathways Precipitate and Sustain Asthma Exacerbations in Children

Subrata

Bizzintino

Mamessier

et al. 2009

The Journal of Immunology

188

172

View full text Add to dashboard Cite

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“…The amount of FceRIg chain in DCs correlates with the surface expression of this receptor, 16 and differential FceRIg chain expression has been shown in atopic vs non-atopic donors. 17 If synthesis of the g chain is upregulated in VKC patients, this might contribute to the increase in FceRI expression.…”

Section: Discussionmentioning

confidence: 99%

Characterization of dendritic cell phenotype in allergic conjunctiva: increased expression of FcɛRI, the high-affinity receptor for immunoglobulin E

Manzouri

Ohbayashi

Leonardi

et al. 2008

Eye

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Purpose Dendritic cells (DCs) express the high-affinity receptor for IgE (FceRI) on their surface, which may enhance their ability to capture and internalize antigens for presentation to T-lymphocytes. The aim of this study was to determine if expression of FceRI þ DCs is increased in the conjunctivae of vernal keratoconjunctivitis (VKC) patients compared with those of normal controls. Methods Conjunctival biopsies were obtained from non-atopic and VKC patients. Double immunohistochemical staining was carried out using antibodies against FceRI and the CD1a antigen, a DC marker. The doublepositive cells were counted in five representative fields of view for each conjunctival sample. Results FceRI þ CD1a þ cells were present in significantly higher numbers in VKC conjunctivae compared with normal controls (mean cell count of 21.3 in VKC vs 5.0 in controls, Po0.005). In normal patients the FceRI-expressing DCs tended to be confined to the epithelial layer or the superficial substantia propria, but in the VKC samples these FceRI þ cells were mainly concentrated in the deeper substantia propria. Conclusions FceRI þ DC numbers are elevated in the conjunctivae of VKC patients, a finding consistent with the results of other studies focusing on atopic conditions. Elevated expression of FceRI on DCs would facilitate antigen presentation and enhance T-cell priming, thereby contributing to ocular symptoms.

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“…Ligation of the high-affinity Fc[RI on the effector cells can induce cell activation and immediate release of inflammatory mediator. 10 The prevalence of atopy in Western countries is about 20-45% and it becomes the main cause of chronic diseases among children.…”

Section: Introductionmentioning

confidence: 99%

Association between atopy and allergic contact dermatitis in Dr. Sardjito General Hospital Yogyakarta

2013

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Association between atopy and development of allergic contact dermatitis (ACD) remains controversial. T cell disfunctions in a patient with atopy complicate the process of nickel sensitization. On the other, the decrease of the skin barrier function and overexpression of Langerhans cells in the patient facilitate the sensitization. This study aimed to evaluate the association between atopy and incidence of nickel ACD. A case-control study was carried out in Allergic and Immunology Sub Department of Dermato-Venereology Policlinic, Dr. Sardjito General Hospital, Yogyakarta, involving 54 nickel ACD patients as case group and 74 healthy subjects as control group. All subjects underwent prick test allergens i.e. house dust, dust mite, cockroach, mixed fungi, nuts and egg white. The skin reaction was considered as a positive result if a wheal diameter of at least 3 mm larger than the negative control or a minimum of half of the positive control. The relationship between atopy and the nickel ACD incidence was analyzed using Chi-Square test with confidence interval (CI) of 95%. A significant association between atopy and the nickel ACD incidence was observed in this study. Subjects with atopy to 1 allergen had risk of nickel ACD 3.74 higher than subjects without atopy (odds ratio/ OR=3.74; 95%CI = 1.64-8.53). Furtheremore, subjects with atopy to 2 allergens had risk of nickel ACD 3.74 higher than subjects without atopy (OR=2.08; 95%CI = 1.01-4.29). In conclusion, atopy is a risk factor of nickel ACD. ABSTRAKHubungan antara atopi dan munculnya dermatitis kontak alergi (DKA) masih kontroversial. Pada penderita atopi terjadi gangguan fungsi sel T yang menghambat proses sensitisasi nikel. Di sisi lain, fungsi sawar kulit penderita atopi menurun dan terjadi ekspresi berlebih sel Langerhans yang mempermudah sensitisasi. Penelitian ini bertujuan untuk mengkaji hubungan antara atopi dan kejadian DKA nikel. Penelitian menggunakan rancangan kasus kontrol dilakukan di Divisi Alergi dan Imunologi, Poliklinik Kulit dan Kelamin, Rumah Sakit Umum Dr. Sardjito Yogyakarta yang melibatkan 54 pasien DKA nikel positif sebagai kelompok kasus dan 74 sukarelawan sehat sebagai kelompok kontrol. Semua subjek menjalai tes tusuk dengan beberap alergen yaitu debu rumah, tungau debu, kecoa, mixed fungi, kacang tanah dan putih telur. Hasil tes dikatakan positif bila diameter reaksi kulit e" 3 mm dari kontrol negatif atau separo dari kontrol positif. Hubungan antara atopi dengan kejadian DKA nikel dianalisis menggunakan uji Chi-Square dengan taraf kepercayaan 95%. Hubungan nyata antara atopi dengan kejadian DKA nikel ditemukan dalam penelitian ini. Subjek dengan atopi terhadap 1 alergen mempunyai risiko DKA nikel 3,74 lebih tinggi dibandingkan dengan subjek tanpa atopi (OR=3,74; 95%CI = 1,64-8,53). Selanjutnya subjek dengan atopi terhadap  2 alergen mempunyai risiko DKA nikel 2,08 lebih tinggi dibandingkan dengan subjek tanpa atopi (OR=2,08; 95%CI = 1,01-4,29). Dapat disimpulkan bahwa atopi merupakan faktor risiko DKA nikel.

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Evidence for a differential expression of the FcεRIγ chain in dendritic cells of atopic and nonatopic donors

Cited by 69 publications

References 45 publications

Interactions between Innate Antiviral and Atopic Immunoinflammatory Pathways Precipitate and Sustain Asthma Exacerbations in Children

Interactions between Innate Antiviral and Atopic Immunoinflammatory Pathways Precipitate and Sustain Asthma Exacerbations in Children

Characterization of dendritic cell phenotype in allergic conjunctiva: increased expression of FcɛRI, the high-affinity receptor for immunoglobulin E

Association between atopy and allergic contact dermatitis in Dr. Sardjito General Hospital Yogyakarta

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