Immunohistochemical investigation of evolving inflammation in lesions of acne vulgaris

被引:55
作者
Layton, AM
Morris, C
Cunliffe, WJ
Ingham, E [1 ]
机构
[1] Univ Leeds, Dept Microbiol, Leeds LS2 9JT, W Yorkshire, England
[2] Univ Leeds, Dept Dermatol, Skin Res Ctr, Leeds LS2 9JT, W Yorkshire, England
关键词
acne; inflammation; CD4 positive T cells;
D O I
10.1111/j.1600-0625.1998.tb00323.x
中图分类号
R75 [皮肤病学与性病学];
学科分类号
100206 ;
摘要
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 CD1, 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.
引用
收藏
页码:191 / 197
页数:7
相关论文
共 20 条
[1]   KERATINOCYTES AS INITIATORS OF INFLAMMATION [J].
BARKER, JNWN ;
MITRA, RS ;
GRIFFITHS, CEM ;
DIXIT, VM ;
NICKOLOFF, BJ .
LANCET, 1991, 337 (8735) :211-214
[2]   THE ASSESSMENT OF ACNE-VULGARIS - THE LEEDS TECHNIQUE [J].
BURKE, BM ;
CUNLIFFE, WJ .
BRITISH JOURNAL OF DERMATOLOGY, 1984, 111 (01) :83-92
[3]   INTRADERMAL INJECTION OF PROPIONIBACTERIUM-ACNES - A MODEL OF INFLAMMATION RELEVANT TO ACNE [J].
DEYOUNG, LM ;
YOUNG, JM ;
BALLARON, SJ ;
SPIRES, DA ;
PUHVEL, SM .
JOURNAL OF INVESTIGATIVE DERMATOLOGY, 1984, 83 (05) :394-398
[4]  
DOLITSKY C, 1989, ACNE RELATED DISORDE, P77
[5]   ADHESION OF T-LYMPHOBLASTS TO EPIDERMAL-KERATINOCYTES IS REGULATED BY INTERFERON-GAMMA AND IS MEDIATED BY INTERCELLULAR-ADHESION MOLECULE-1 (ICAM-1) [J].
DUSTIN, ML ;
SINGER, KH ;
TUCK, DT ;
SPRINGER, TA .
JOURNAL OF EXPERIMENTAL MEDICINE, 1988, 167 (04) :1323-1340
[6]   LYMPHOCYTE FUNCTION ASSOCIATED ANTIGEN-1 (LFA-1) INTERACTION WITH INTERCELLULAR-ADHESION MOLECULE-1 (ICAM-1) IS ONE OF AT LEAST 3 MECHANISMS FOR LYMPHOCYTE ADHESION TO CULTURED ENDOTHELIAL-CELLS [J].
DUSTIN, ML ;
SPRINGER, TA .
JOURNAL OF CELL BIOLOGY, 1988, 107 (01) :321-331
[7]  
DUSTIN ML, 1986, J IMMUNOL, V137, P245
[8]   NEUTROPHIL CHEMOTAXIS IN PATIENTS WITH ACNE RECEIVING ORAL TETRACYCLINE THERAPY [J].
ESTERLY, NB ;
KORANSKY, JS ;
FUREY, NL ;
TREVISAN, M .
ARCHIVES OF DERMATOLOGY, 1984, 120 (10) :1308-1313
[9]   CHARACTERIZATION OF INTERCELLULAR-ADHESION MOLECULE-1 AND HLA-DR EXPRESSION IN NORMAL AND INFLAMED SKIN - MODULATION BY RECOMBINANT GAMMA INTERFERON AND TUMOR NECROSIS FACTOR [J].
GRIFFITHS, CEM ;
VOORHEES, JJ ;
NICKOLOFF, BJ .
JOURNAL OF THE AMERICAN ACADEMY OF DERMATOLOGY, 1989, 20 (04) :617-629
[10]   PRO-INFLAMMATORY LEVELS OF INTERLEUKIN-1-ALPHA-LIKE BIOACTIVITY ARE PRESENT IN THE MAJORITY OF OPEN COMEDONES IN ACNE-VULGARIS [J].
INGHAM, E ;
EADY, EA ;
GOODWIN, CE ;
COVE, JH ;
CUNLIFFE, WJ .
JOURNAL OF INVESTIGATIVE DERMATOLOGY, 1992, 98 (06) :895-901