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 language | English |
|---|---|
| Pages (from-to) | 497-504 |
| Number of pages | 8 |
| Journal | Archivum Immunologiae et Therapiae Experimentalis |
| Volume | 48 |
| Issue number | 6 |
| Publication status | Published - 2000 |
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Keywords
- Atopy
- Dendritic cells
- Keratinocytes
- Skin
- T lymphocytes
ASJC Scopus subject areas
- Immunology
Cite this
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 journal › Article
}
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
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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 -