Langerhans’ Cells and L1 Antigen Expression in Normal and Abnormal Squamous Epithelium of the Cervical Transformation Zone

Abstract

This study evaluates the presence of Langerhans’ cells and expression of L1 antigen in squamous epithelium of the normal and dysplastic transformation zone of the cervix uteri and determines the influence of tobacco smoking and pregnancy. Women who smoked and pregnant women showed a decrease of Langerhans’ cell counts in normal epithelium. In cervical intraepithelial neoplasia (CIN) 1 lesions, decreased Langerhans’ cell counts were noted. L1 antigen expression was significantly less in CIN of all grades. Normal squamous epithelium of smokers showed weaker staining for L1 antigen but total staining scores were not significantly different. These data suggest a decrease in epithelial cell-mediated immune response in smokers, pregnant women and in low-grade CIN. Dysplastic squamous cells probably have intracellular regulatory problems independent of other immune cells.

Langerhans Cells in Cervical Intraepithelial Neoplasia Related to Smoking Habits

“…Our results were similar to others mentioned in the literature [11,13]. It was not the objective of this study to compare the number of cervical epithelium Langerhans cells of healthy women with that of women presenting with CIN 3.…”

Prevalence of micronuclei in exfoliated uterine cervical cells from patients with risk factors for cervical cancer

“…30 These effects may result from decreased numbers of Langerhans cells in the cervix of women who smoke. 31 Women who consume alcohol are considered to present a high and progressive risk of developing in situ and invasive cervical and vaginal cancer. Epidemiological data have suggested a direct link between alcoholism and lifestyle factors such as promiscuity, smoking, use of hormonal contraceptives and dietary deficiencies.…”

Long-Term Administration of Intravaginal Dehydroepiandrosterone on Regression of Low-Grade Cervical Dysplasia – A Pilot Study

“…Even in the absence of immunosuppression, recent studies have confirmed that cervical dysplasia develops in those individuals whose immune systems are unable to clear HPV, resulting in persistent infection [4,5]. Among cigarette smokers, a decrease in the numbers of Langerhans' cells and CD4 cells in cervical stroma was demonstrated [6,7], suggesting that the increased risk of dysplasia seen in association with tobacco use may be due, at least in part, from local immune suppression. The regression of early dysplasia, therefore, appears to depend on the ability of the immune system to eradicate virally infected hyperproliferative cells.…”