MHC class II expression by follicular keratinocytes in canine demodicosis--an immunohistochemical study.
Vet Immunol Immunopathol
; 118(3-4): 210-20, 2007 Aug 15.
Article
in En
| MEDLINE
| ID: mdl-17604845
MHC class II proteins present fragments of extra cellular antigen to stimulate CD4(+) T lymphocytes. Aim of this study was the detection of MHC class II antigens on different cutaneous cells in canine demodicosis. Histopathological and immunohistochemical examination of skin biopsies from 44 dogs with demodicosis is reported. The control group consisted of skin biopsies taken from 10 necropsied dogs without obvious skin lesions. The immunohistological assessment of the MHC class II expression revealed MHC class II proteins on different cell types of infiltrating inflammatory cells, i.e. APCs (antigen-presenting cells), macrophages, T lymphocytes and B lymphocytes. The plasma cells, however, only showed expression in 32 (73%) of 44 cases. Generally it was noticeable that most plasma cells but never all of them expressed MHC class II. Neutrophils, mast cells and eosinophils were MHC class II negative. Furthermore, in 39 biopsies (89%) from dogs with demodicosis MHC class II positive follicular keratinocytes were found. The control group did not show MHC class II expression on epithelial cells. Concerning the endothelial cells, a total of 25 biopsies (57%) showed MHC class II expression in which different vascular plexuses were affected by staining. This examination shows that MHC class II expression in the skin of dogs suffering form demodicosis is elevated. Especially the MHC class II expression by follicular keratinocytes seems to be conspicuous. We hypothesize that this is in association with the development and the maintenance of follicular inflammation.
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Collection:
01-internacional
Database:
MEDLINE
Main subject:
Immunohistochemistry
/
Histocompatibility Antigens Class II
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Keratinocytes
/
Gene Expression Regulation
/
Dog Diseases
/
Mite Infestations
Limits:
Animals
Language:
En
Journal:
Vet Immunol Immunopathol
Year:
2007
Document type:
Article
Affiliation country:
Country of publication: