Both Pimecrolimus and Corticosteroids Deplete Plasmacytoid Dendritic Cells in Patients with Atopic Dermatitis

Hoetzenecker, Wolfram; Meindl, Simone; Stuetz, Anton; Stingl, Georg; Elbe‐Bürger, Adelheid

doi:10.1038/sj.jid.5700368

Cited by 14 publications

(12 citation statements)

References 21 publications

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“…An increased maturational response of pDCs in severe COPD, as suggested by FREEMAN et al [17], could also explain the lower numbers of BDCA-2-positive pDCs. Finally, the use of inhaled and systemic corticosteroids by patients with severe and very severe COPD could contribute to the reduced number of pDCs in this study, as these drugs are known to induce apoptosis in circulating and tissue-resident pDCs [36][37][38][39]. This lower number of pDCs in lymphoid follicles of patients with very severe COPD treated with inhaled steroids could be linked to the observed association of increased risk of pneumonia and the use of inhaled corticosteroids in patients with COPD [40].…”

Section: Discussionmentioning

confidence: 77%

Plasmacytoid dendritic cells in pulmonary lymphoid follicles of patients with COPD

Pottelberge¹,

Bracke²,

Broeck³

et al. 2010

European Respiratory Journal

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Plasmacytoid dendritic cells (pDCs) are professional antigen-presenting cells with antiviral and tolerogenic capabilities. Viral infections and autoimmunity are proposed to be important mechanisms in the pathogenesis of chronic obstructive pulmonary disease (COPD).The study aimed to quantify blood dendritic cell antigen 2-positive pDCs in lungs of subjects with or without COPD by immunohistochemistry and flow cytometry, combined with the investigation of the influence of cigarette smoke extract (CSE) on the function of pDCs in vitro.pDCs were mainly located in lymphoid follicles, a finding compatible with their expression of lymphoid homing chemokine receptors CXCR3 and CXCR4. pDC accumulated in the lymphoid follicles and in lung digests of patients with mild to moderate COPD, compared with smokers without airflow limitation and patients with COPD Global Initiative for Chronic Obstructive Lung disease (GOLD) stage III-IV. Exposing maturing pDC of healthy subjects to CSE in vitro revealed an attenuation of the expression of co-stimulatory molecules and impaired interferon-a production. Maturing pDC from patients with COPD produced higher levels of tumour necrosis factor (TNF)-a and interleukin (IL)-8 compared to pDC from healthy subjects.CSE significantly impairs the antiviral function of pDCs. In COPD, a GOLD stage dependent accumulation of pDC in lymphoid follicles is present, combined with an enhanced production of TNF-a and IL-8 by maturing pDCs.

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Section: Discussionmentioning

confidence: 77%

Plasmacytoid dendritic cells in pulmonary lymphoid follicles of patients with COPD

Pottelberge¹,

Bracke²,

Broeck³

et al. 2010

European Respiratory Journal

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“…As the dose of glucocorticoids is tapered, the DC numbers gradually recover. Patients and healthy volunteers treated with corticosteroids show a decrease in the levels of circulating pDCs (45). It has been shown that glucocorticoid treatment of human pDCs can induce apoptosis via the extrinsic pathway (46).…”

Section: Regulation Of DC Apoptosismentioning

confidence: 99%

Dendritic Cell Apoptosis: Regulation of Tolerance versus Immunity

Kushwah

2010

The Journal of Immunology

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Dendritic cell (DC) apoptosis is an important event that regulates the balance between tolerance and immunity through multiple pathways, and defects in DC apoptosis can trigger autoimmunity. DC apoptosis is also associated with immunosuppression and has been observed under several pathologies and infections. Recent studies indicate that apoptotic DCs can also play an active role in induction of tolerance. This review discusses the regulatory pathways of DC apoptosis, stimuli inducing DC apoptosis, and the implications of DC apoptosis in the induction of immunosuppression and/or tolerance.

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“…Having stated the central role of topical corticosteroids, we must also recognize the substantial benefits we gained from topical calcineurin inhibitors [140][141][142][143][144][145][146][147][148][149]. In the last few years, the medical community has gained much understanding on this group of medications regarding its desirable actions and potential side effects [140][141][142][143][144][145][146][147][148][149].…”

Section: Therapeutic Advancesmentioning

confidence: 99%

“…In the last few years, the medical community has gained much understanding on this group of medications regarding its desirable actions and potential side effects [140][141][142][143][144][145][146][147][148][149]. Specifically, these inhibitors improved skin inflammation in patients with atopic dermatitis, likely through the mechanisms of regulatory T cell correction [141], depletion of plasmacytoid dendritic cells [142], suppressing expressions of the cytokine IL-5, the chemokines eotaxin and RANTES, and the chemokine receptor CCR3 [145], induction of apoptosismediated T cell depletion [146], reduction of dermal infiltration of cytokineexpressing inflammatory cells [147,148], and suppression of skin response to aeroallergens [143], while at the same time they do not appear to hinder the immune system to respond to vaccination [140,149]. The recent 'black box' warning label placed by the FDA on these inhibitors casts a cloud for the longterm use of this group of medications.…”

Section: Therapeutic Advancesmentioning

confidence: 99%

Atopic Dermatitis in 2008

Chan¹

2008

Current Directions in Autoimmunity

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Atopic dermatitis (also termed atopic eczema and infantile eczema), a chronic, itchy, inflammatory skin disease that sets on at infancy or early childhood, is observed with increasing prevalence around the world, particularly in developed nations. Although sufficient evidences are not yet available to define it as a classical autoimmune disease, autoantigens have been identified. Investigations of atopic dermatitis in human patients and animal models suggest that this disease is initiated, maintained and perpetuated by the actions of cytokines, chemokines, T cells, antigen-presenting cells and other inflammatory cells; there is also evidence of skin barrier defect and angiogenesis. Recent identification of mutations of the epidermal barrier protein filaggrin (encoded by FLG), present in about 9% of people of European origin, with 70% of individuals homozygous or compound heterozygous for FLG null alleles developing atopic dermatitis, provides a strong link between a defect of the epidermal barrier that allows easy penetration of pathogen/allergen through the skin and a systemic hyperactive immune response to the penetrated pathogen/allergen. The newly introduced concept of 'intrinsic' and 'extrinsic' atopic dermatitis has fueled the debate among academic dermatologists as to how 'atopic' atopic dermatitis should be defined. Some recent advancements on the management options for atopic dermatitis are also discussed.

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Both Pimecrolimus and Corticosteroids Deplete Plasmacytoid Dendritic Cells in Patients with Atopic Dermatitis

Cited by 14 publications

References 21 publications

Plasmacytoid dendritic cells in pulmonary lymphoid follicles of patients with COPD

Plasmacytoid dendritic cells in pulmonary lymphoid follicles of patients with COPD

Dendritic Cell Apoptosis: Regulation of Tolerance versus Immunity

Atopic Dermatitis in 2008

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