Am. Layton et al., IMMUNOHISTOCHEMICAL INVESTIGATION OF EVOLVING INFLAMMATION IN LESIONSOF ACNE-VULGARIS, Experimental dermatology, 7(4), 1998, pp. 191-197
The mechanisms involved in the development of inflammation in acne vul
garis have yet to be elucidated. Previous studies have shown that the
initial cellular infiltrate in early inflammatory lesions is mononucle
ar, predominantly CD4 positive T cells. The aims of this study were to
investigate the pattern of expression of adhesion molecules and HLA-D
R in evolving acne lesions. Forty-nine patients with moderate to sever
e acne were biopsied following lesion mapping. Lesions were classified
according to their duration of inflammation as up to 6 h, from 6 to 2
4 h, from 24 to 48 h and from 48 to 72 h. The cellular infiltrate was
determined using monoclonal antibodies to CD1, CD3, CD4 and CD8. The e
xpression of ICAM-1, E-selectin, VCAM-1 and HLA-DR was determined. Ear
ly (6 h) lesions had perivascular CD3 positive T-cell infiltrates whic
h were predominantly CD4 positive. This was associated with vascular e
xpression of ICAM-1, E-selectin, VCAM-1 and HLA-DR. Periductal infiltr
ates were present in 70% of the early lesions (up to 6 h). The cells w
ere 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 i
n early and late lesions. CD1 positive cells were a minor, but consist
ent element in the perivascular and periductal infiltrates of early an
d late lesions. There was no statistically significant difference in t
he levels of expression of E-selectin, VCAM-1, ICAM-1 or HLA-DR for le
sions of different duration. The pattern of HLA-DR and adhesion molecu
le expression plus the nature of the cellular infiltrate supports the
hypothesis that inflammation in acne is mediated by CD4 positive T cel
ls.