Pathogenetic mechanisms of atopic dermatitis

Saveria Pastore, Francesca Mascia, Maria Laura Giustizieri, Alberto Giannetti, Giampiero Girolomoni

Research output: Contribution to journalArticle

Abstract

Atopic dermatitis (AD) is a chronic inflammatory disease which results from complex interactions between genetic and environmental mechanisms. An altered lipid composition of the stratum corneum is responsible for the xerotic aspect of the skin and determines a higher permeability to allergens and irritants. Keratinocytes of AD patients exhibit a propensity to an exaggerated production of cytokines and chemokines, a phenomenon that can have a major role in promoting and maintaining inflammation. Specific immune responses against a variety of environmental allergens are also implicated in AD pathogenesis, with a bias towards Th2 immune responses. In particular, dendritic cells expressing membrane IgE receptors play a critical role in the amplification of allergen-specific T cell responses. Cross-linkage of specific IgE receptors on dermal mast cells provokes the release and synthesis of a vast series of mediators. Following their recruitment and activation into the skin, eosinophils are also thought to contribute relevantly to tissue damage. Thus, a complex network of cytokines and chemokines contributes to establishing a local milieu that favors the permanence of inflammation in AD skin.

Original languageEnglish
Pages (from-to)497-504
Number of pages8
JournalArchivum Immunologiae et Therapiae Experimentalis
Volume48
Issue number6
Publication statusPublished - 2000

Fingerprint

Atopic Dermatitis
Allergens
IgE Receptors
Skin
Chemokines
Cytokines
Inflammation
Irritants
Keratinocytes
Eosinophils
Mast Cells
Cornea
Dendritic Cells
Permeability
Chronic Disease
Cell Membrane
T-Lymphocytes
Lipids

Keywords

  • Atopy
  • Dendritic cells
  • Keratinocytes
  • Skin
  • T lymphocytes

ASJC Scopus subject areas

  • Immunology

Cite this

Pastore, S., Mascia, F., Giustizieri, M. L., Giannetti, A., & Girolomoni, G. (2000). Pathogenetic mechanisms of atopic dermatitis. Archivum Immunologiae et Therapiae Experimentalis, 48(6), 497-504.

Pathogenetic mechanisms of atopic dermatitis. / Pastore, Saveria; Mascia, Francesca; Giustizieri, Maria Laura; Giannetti, Alberto; Girolomoni, Giampiero.

In: Archivum Immunologiae et Therapiae Experimentalis, Vol. 48, No. 6, 2000, p. 497-504.

Research output: Contribution to journalArticle

Pastore, S, Mascia, F, Giustizieri, ML, Giannetti, A & Girolomoni, G 2000, 'Pathogenetic mechanisms of atopic dermatitis', Archivum Immunologiae et Therapiae Experimentalis, vol. 48, no. 6, pp. 497-504.
Pastore S, Mascia F, Giustizieri ML, Giannetti A, Girolomoni G. Pathogenetic mechanisms of atopic dermatitis. Archivum Immunologiae et Therapiae Experimentalis. 2000;48(6):497-504.
Pastore, Saveria ; Mascia, Francesca ; Giustizieri, Maria Laura ; Giannetti, Alberto ; Girolomoni, Giampiero. / Pathogenetic mechanisms of atopic dermatitis. In: Archivum Immunologiae et Therapiae Experimentalis. 2000 ; Vol. 48, No. 6. pp. 497-504.
@article{5cf9ab59462e45b888abfbc3279f5f22,
title = "Pathogenetic mechanisms of atopic dermatitis",
abstract = "Atopic dermatitis (AD) is a chronic inflammatory disease which results from complex interactions between genetic and environmental mechanisms. An altered lipid composition of the stratum corneum is responsible for the xerotic aspect of the skin and determines a higher permeability to allergens and irritants. Keratinocytes of AD patients exhibit a propensity to an exaggerated production of cytokines and chemokines, a phenomenon that can have a major role in promoting and maintaining inflammation. Specific immune responses against a variety of environmental allergens are also implicated in AD pathogenesis, with a bias towards Th2 immune responses. In particular, dendritic cells expressing membrane IgE receptors play a critical role in the amplification of allergen-specific T cell responses. Cross-linkage of specific IgE receptors on dermal mast cells provokes the release and synthesis of a vast series of mediators. Following their recruitment and activation into the skin, eosinophils are also thought to contribute relevantly to tissue damage. Thus, a complex network of cytokines and chemokines contributes to establishing a local milieu that favors the permanence of inflammation in AD skin.",
keywords = "Atopy, Dendritic cells, Keratinocytes, Skin, T lymphocytes",
author = "Saveria Pastore and Francesca Mascia and Giustizieri, {Maria Laura} and Alberto Giannetti and Giampiero Girolomoni",
year = "2000",
language = "English",
volume = "48",
pages = "497--504",
journal = "Archivum Immunologiae et Therapiae Experimentalis",
issn = "0004-069X",
publisher = "Birkhauser Verlag Basel",
number = "6",

}

TY - JOUR

T1 - Pathogenetic mechanisms of atopic dermatitis

AU - Pastore, Saveria

AU - Mascia, Francesca

AU - Giustizieri, Maria Laura

AU - Giannetti, Alberto

AU - Girolomoni, Giampiero

PY - 2000

Y1 - 2000

N2 - Atopic dermatitis (AD) is a chronic inflammatory disease which results from complex interactions between genetic and environmental mechanisms. An altered lipid composition of the stratum corneum is responsible for the xerotic aspect of the skin and determines a higher permeability to allergens and irritants. Keratinocytes of AD patients exhibit a propensity to an exaggerated production of cytokines and chemokines, a phenomenon that can have a major role in promoting and maintaining inflammation. Specific immune responses against a variety of environmental allergens are also implicated in AD pathogenesis, with a bias towards Th2 immune responses. In particular, dendritic cells expressing membrane IgE receptors play a critical role in the amplification of allergen-specific T cell responses. Cross-linkage of specific IgE receptors on dermal mast cells provokes the release and synthesis of a vast series of mediators. Following their recruitment and activation into the skin, eosinophils are also thought to contribute relevantly to tissue damage. Thus, a complex network of cytokines and chemokines contributes to establishing a local milieu that favors the permanence of inflammation in AD skin.

AB - Atopic dermatitis (AD) is a chronic inflammatory disease which results from complex interactions between genetic and environmental mechanisms. An altered lipid composition of the stratum corneum is responsible for the xerotic aspect of the skin and determines a higher permeability to allergens and irritants. Keratinocytes of AD patients exhibit a propensity to an exaggerated production of cytokines and chemokines, a phenomenon that can have a major role in promoting and maintaining inflammation. Specific immune responses against a variety of environmental allergens are also implicated in AD pathogenesis, with a bias towards Th2 immune responses. In particular, dendritic cells expressing membrane IgE receptors play a critical role in the amplification of allergen-specific T cell responses. Cross-linkage of specific IgE receptors on dermal mast cells provokes the release and synthesis of a vast series of mediators. Following their recruitment and activation into the skin, eosinophils are also thought to contribute relevantly to tissue damage. Thus, a complex network of cytokines and chemokines contributes to establishing a local milieu that favors the permanence of inflammation in AD skin.

KW - Atopy

KW - Dendritic cells

KW - Keratinocytes

KW - Skin

KW - T lymphocytes

UR - http://www.scopus.com/inward/record.url?scp=0034569170&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0034569170&partnerID=8YFLogxK

M3 - Article

C2 - 11197604

AN - SCOPUS:0034569170

VL - 48

SP - 497

EP - 504

JO - Archivum Immunologiae et Therapiae Experimentalis

JF - Archivum Immunologiae et Therapiae Experimentalis

SN - 0004-069X

IS - 6

ER -