CD1a+, CD3+, CD4+, CD8+, CD68+and cutaneous lymphocyte-associated antigen-positive cells in Bowen's disease

Citation
H. Duan et al., CD1a+, CD3+, CD4+, CD8+, CD68+and cutaneous lymphocyte-associated antigen-positive cells in Bowen's disease, BR J DERM, 143(6), 2000, pp. 1211-1216
Citations number
20
Categorie Soggetti
Dermatology,"da verificare
Journal title
BRITISH JOURNAL OF DERMATOLOGY
ISSN journal
00070963 → ACNP
Volume
143
Issue
6
Year of publication
2000
Pages
1211 - 1216
Database
ISI
SICI code
0007-0963(200012)143:6<1211:CCCCCC>2.0.ZU;2-#
Abstract
Background Bowen's disease (BD) is a squamous cell carcinoma in situ that r arely invades into the underlying dermis, However, little is known about it s immunohistology. Objectives To evaluate the relationship between the cytological properties of the tumour cells in ED and the host immune response. Methods We examined the expression of p53, proliferating cell nuclear antig en (PCNA) and Ki67 antigen, and the number of mitotic cells, together with the number of intratumoral and dermal infiltrating CD1a+, CD3+, CD4+, CD8+, CD68+ and cutaneous lymphocyte-associated antigen (CLA)+ cells in 18 cases of genital ED. Results When compared with normal genital skin (n = 10), there was a signif icantly higher number of mitotic cells as well as higher expression of p53, PCNA+ and Ki67+ cells in BD. There was significant mutual correlation bet ween CD3+, CD4+ and CD68+ cells in the tumoral epidermis. The number of CD1 a+ Langerhans cells significantly decreased in ED epidermis; however, derma l CD1a+ cells were increased, Interestingly numbers of dermal CD1a+ cells s ignificantly correlated with those of intratumoral CD3+, CD4+ and CD68+ cel ls. In situ hybridization for human papillomavirus (HPV) demonstrated that HPV-infected ED had significantly less infiltration of intratumoral CD3+ ce lls and CLA+ cells. Conclusions The present data suggest that dermal CD1a+ cells may participat e in the immune surveillance and that HPV infection may interfere with the intratumoral infiltration of CLA+ cells in ED.