Immunohistochemical investigation of evolving inflammation in lesions of acne vulgaris.
The mechanisms involved in the development of inflammation in acne vulgaris have yet to be elucidated. Previous studies have shown that the initial cellular infiltrate in early inflammatory lesions is mononuclear, predominantly CD4 positive T cells. The aims of this study were to investigate the pattern of expression of adhesion molecules and HLA-DR in evolving acne lesions. Forty-nine patients with moderate to severe acne were biopsied following lesion mapping. Lesions were classified according to their duration of inflammation as up to 6 h, from 6 to 24 h, from 24 to 48 h and from 48 to 72 h. The cellular infiltrate was determined using monoclonal antibodies to CDI, CD3, CD4 and CD8. The expression of ICAM-1, E-selectin. VCAM-1 and HLA-DR was determined. Early (6 h) lesions had perivascular CD3 positive T-cell infiltrates which were predominantly CD4 positive. This was associated with vascular expression of ICAM-1, E-selectin, VCAM-1 and HLA-DR. Periductal infiltrates were present in 70% of the early lesions (up to 6 h). The cells were predominantly CD4 positive and associated with a high level of HLA-DR and ICAM-1 expression. Periductal infiltration increased with time and persisted to 72 h. ICAM-1 and HLA-DR were expressed epidermally in early and late lesions. CD1 positive cells were a minor, but consistent element in the perivascular and periductal infiltrates of early and late lesions. There was no statistically significant difference in the levels of expression of E-selectin, VCAM-1, ICAM-1 or HLA-DR for lesions of different duration. The pattern of HLA-DR and adhesion molecule expression plus the nature of the cellular infiltrate supports the hypothesis that inflammation in acne is mediated by CD4 positive T cells.
Department of Dermatology, University of Leeds, UK.
A M
AM
Layton
C
C
Morris
W J
WJ
Cunliffe
E
E
Ingham
D000152:Acne Vulgaris / Q000276:immunology*; D000293:Adolescent; D000328:Adult; D015703:Antigens, CD / Q000096:biosynthesis* / Q000276:immunology; D015815:Cell Adhesion Molecules / Q000096:biosynthesis* / Q000276:immunology; D005260:Female; D006684:HLA-DR Antigens / Q000096:biosynthesis* / Q000276:immunology; D006801:Humans; D007150:Immunohistochemistry; D007249:Inflammation / Q000276:immunology* / Q000473:pathology; D008297:Male
D015703:Antigens, CD; D015815:Cell Adhesion Molecules; D006684:HLA-DR Antigens