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European Journal of Dermatology
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publication venue for: An immunohistochemical study of UV-induced skin lesions in actinic prurigo. Resistance of Langerhans cells to UV light

An immunohistochemical study of UV-induced skin lesions in actinic prurigo. Resistance of Langerhans cells to UV light
related by: authorship 2976
related by: authorship 2970
date time value: article date 627
type: Entity
volume: 8
type: Continuant
page start: 24
chemicalscas: Antibodies, Monoclonal; Cell Adhesion Molecules; Intercellular Adhesion Molecule-1, 126547-89-5; Vascular Cell Adhesion Molecule-1
type: Article
related by: authorship 2972
type: Generically Dependent Continuant
most specific type: Article
type: Document
issue: 1
type: Information Content Entity
related by: authorship 2974
page end: 28
e iscopus: 2-s2.0-0031800743
estado: published
pmid: 9649710
abstract: Actinic prurigo is an inflammatory disease of the skin that appears to be mediated by an abnormal immune response. Cell adhesion molecules play a key role in the induction of the immune response as well as in the pathogenesis of inflammation. We investigated the expression of cell adhesion and activation molecules, as well as the density of Langerhans cells in skin from patients with actinic prurigo. Skin biopsies from ultraviolet light- induced lesions, and non-irradiated areas from 10 actinic prurigo patients were studied; in addition, several spontaneous skin lesions were studied. Skiff biopsies from normal individuals were used as controls. The expression of ICAM-1, ICAM-3, LFA-3, CD2, LFA-1, VLA-4, CD1a, VCAM-1, CD69, and activated b1 integrins were assessed by immunostaining. An increased expression of LFA-1, LFA-2, ICAM-3, VLA-4, and activated b1 integrins was observed in the cell infiltrate of actinic prurigo lesions and an up- regulated expression of ICAM-1 was detected in keratinocytes from these specimens. Interestingly, the number of Langerhans cells (CD1a ) in actinic prurigo skin was not significantly affected by ultraviolet irradiation, a phenomenon that was not observed in normal controls. The increased expression of adhesion molecules in the cell infiltrate of actinic prurigo, indicates that these cells are activated and suggests that they are involved in the skin damage seen in these patients. The resistance of Langerhans cells from patients with actinic prurigo to ultraviolet light may have an important role in the pathogenesis of this condition. The involvement of keratinocytes in the pathogenesis of actinic prurigo is suggested by the expression of ICAM-1 on these cells.
has publication venue: European Journal of Dermatology
related by: authorship 2977
related by: authorship 2971
origen: scopus
freetext keyword: Actinic prurigo; CD69; Cell adhesion molecules; Langerhans cells beta1 integrin; CD1 antigen; CD2 antigen; CD69 antigen; cell adhesion molecule; integrin; intercellular adhesion molecule 1; intercellular adhesion molecule 3; lymphocyte function associated antigen 1; lymphocyte function associated antigen 3; vascular cell adhesion molecule 1; antigen expression; article; cell activation; cell density; cell infiltration; clinical article; controlled study; gene expression; human; human cell; human tissue; immune response; immunohistochemistry; inflammation; keratinocyte; Langerhans cell; prurigo; skin biopsy; ultraviolet radiation; Antibodies, Monoclonal; Biopsy, Needle; Cell Adhesion Molecules; Cells, Cultured; Humans; Intercellular Adhesion Molecule-1; Keratinocytes; Langerhans Cells; Prurigo; Reference Values; Ultraviolet Rays; Vascular Cell Adhesion Molecule-1
type: Thing
most specific type: Document
related by: authorship 2973
related by: authorship 2975
crisid: 627
abstract: Actinic prurigo is an inflammatory disease of the skin that appears to be mediated by an abnormal immune response. Cell adhesion molecules play a key role in the induction of the immune response as well as in the pathogenesis of inflammation. We investigated the expression of cell adhesion and activation molecules, as well as the density of Langerhans cells in skin from patients with actinic prurigo. Skin biopsies from ultraviolet light- induced lesions, and non-irradiated areas from 10 actinic prurigo patients were studied; in addition, several spontaneous skin lesions were studied. Skiff biopsies from normal individuals were used as controls. The expression of ICAM-1, ICAM-3, LFA-3, CD2, LFA-1, VLA-4, CD1a, VCAM-1, CD69, and activated b1 integrins were assessed by immunostaining. An increased expression of LFA-1, LFA-2, ICAM-3, VLA-4, and activated b1 integrins was observed in the cell infiltrate of actinic prurigo lesions and an up- regulated expression of ICAM-1 was detected in keratinocytes from these specimens. Interestingly, the number of Langerhans cells (CD1a%2b) in actinic prurigo skin was not significantly affected by ultraviolet irradiation, a phenomenon that was not observed in normal controls. The increased expression of adhesion molecules in the cell infiltrate of actinic prurigo, indicates that these cells are activated and suggests that they are involved in the skin damage seen in these patients. The resistance of Langerhans cells from patients with actinic prurigo to ultraviolet light may have an important role in the pathogenesis of this condition. The involvement of keratinocytes in the pathogenesis of actinic prurigo is suggested by the expression of ICAM-1 on these cells.

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RDF description of An immunohistochemical study of UV-induced skin lesions in actinic prurigo. Resistance of Langerhans cells to UV light - http://orbis.uaslp.mx/vivo/individual/scopus626
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date: 2026-08-24T21:50:55
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