Immune response commonly is cited as a determining factor in the development or clearance of various neoplasias, but the immunobiology of neoplastic progression is poorly understood. The cervix has the largest concentration of lymphocytes found in the female genital tract and as a component of the common mucosal immune system guards against ascending infection from the microbial-laiden vagina, but cervical immunocytes have not been well characterized in the neoplasia itself. The objective of this study is to characterize the subpopulations of lymphocytes that infiltrate various grades of cervical neoplasia including metaplasia to invasive carcinoma. To establish the correlation I examined 60 cases of uterine cervix which were divided 4 categories according to the Bethesda Classification system; normal cervix(15), low grade squamous intraepithelial lesions(SILs)(15), high grade SILs(15), and invasive squamous cell carcinomas(15 cases). The degrees of T-lymphocyte infiltration were assessed after immunohistochemical staining by UCHL1, and compared to stainability of aberrant p53 and bcl-2 protein. There were significant increasing number and proportion of T-cells of invaisve cancers compared with that of preinvasive lesions. Aberrant p53 expression of invasive cancer was a little more intensive than that of low grade and high grade SILs, and there was no correlation between T-cell infiltration and aberrant p53 and/or bcl-2 expression. Bcl-2 was expressed in most of basal layer and some cases of parabasal layer of low and high grade SILs, and some minute foci of invasive cancer. In the adjacent areas of SILs and invasive lesions strong bcl-2 expression was noted in parabasal, intermediate or superficial cells case by case. In conclusion, the UCHLl-positive T cell infiltrate far exceeded in the invasive, but not in the preinvasive lesions, a finding that suggests that T cells are recruited preferentially to cervical lesions with progression to invasion. It is suggested that the T cell recruitment is not related to p53 or bc1-2, but the unknown third factors, and the bcl-2 overexpression is involved in the early step of epithelial neoplastic transforrnation and followed by recurrent overexposure to various oncogenic factors.
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