Back to Search Start Over

Phenotypic characterization of mononuclear cells and class II antigen expression in angular cheilitis infected by Candida albicans or Staphylococcus aureus.

Authors :
Ohman SC
Jontell M
Jonsson R
Source :
Scandinavian journal of dental research [Scand J Dent Res] 1989 Apr; Vol. 97 (2), pp. 178-85.
Publication Year :
1989

Abstract

In the present study we characterized the phenotypes of infiltrating mononuclear cells in angular cheilitis lesions to further explore the pathogenesis of this disorder. Frozen sections from lesions infected by Candida albicans and/or Staphylococcus aureus were subjected to immunohistochemical analysis utilizing monoclonal antibodies directed to subsets of T-lymphocytes, B-lymphocytes, and macrophages. In addition, the expression of Class II antigens (HLA-DP, -DQ, -DR), the interleukin 2- and transferrin-receptors was studied on resident and infiltrating cells. An intense infiltration of T-lymphocytes was accompanied by expression of Class II antigens on the epidermal keratinocytes in lesion infected by Candida albicans. The Staphylococcus aureus infected lesions displayed a diffuse infiltration of T-lymphocytes but virtually no expression of Class II antigen by epidermal keratinocytes. These observations suggest that the cell-mediated arm of the immune system is involved in the inflammatory reaction of lesions infected by Candida albicans. In addition, the present study confirms that epidermal expression of Class II antigens is closely related to the type and magnitude of the infiltrating T-lymphocyte. Finally, these findings indicate that the type of inflammatory reaction in angular cheilitis is primarily dependent on the isolated microorganism, although the clinical pictures of the disorder are virtually identical.

Details

Language :
English
ISSN :
0029-845X
Volume :
97
Issue :
2
Database :
MEDLINE
Journal :
Scandinavian journal of dental research
Publication Type :
Academic Journal
Accession number :
2468179
Full Text :
https://doi.org/10.1111/j.1600-0722.1989.tb01447.x