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HLA Class II Antigen Expression in Human Papillomavirus-associated Cervical Cancer¹

Cancer Research Campaign Department of Immunology, Paterson Institute for Cancer Research, Christie Hospital, Manchester, M20 9BX, United Kingdom [S. S. G., M. D-K., P. L. S.], and Servicio De Analisis Clinicos, Hospital Virgen De Las Nieves, Avenida Coronel Munoz 2, 18014 Granada, Spain [T. C.]

The observation that tumor cells of some neoplasms display major histocompatibility complex (MHC) class II molecules may be of functional significance, influencing the progression of malignancy by allowing the cancer cells to present antigen to the immune system. In the normal cervix, class II molecules are expressed by columnar but not squamous epithelium. The pattern of MHC class II expression in cervical carcinomas has been documented using immunohistochemical methods. Of 53 cervical squamous carcinomas examined for MHC class II expression, only 17% maintained a negative phenotype characteristic of the epithelium from which they were derived, while the remaining tumors exhibited either uniform (45%) or heterogeneous (38%) expression. Tumor areas which were class II positive also express class II associated invariant chain and the adhesion molecules lymphocyte function antigen 3 and intercellular adhesion molecule 1. The DR, DP, and DQ class II MHC subloci are differentially expressed, suggesting independent regulation. There is a trend for tumors with the uniform class II phenotype to predominantly express DR antigen, whereas tumors of the heterogeneous class II phenotype express with equal frequency either DR or DP antigens dominantly. There is no apparent influence of class II status on lymphocyte infiltration of the tumors. The presence of human papillomavirus 16 DNA in the cervical carcinoma specimens was analyzed by Southern blotting of restriction enzyme digested DNA and no correlation between the presence of human papilloma virus and MHC class II expression was found.

¹ This work was supported by the Cancer Research Campaign and a British-Spanish Joint Research Programme Grant, ref/2398.

² Supported by a Joseph Starkey Clinical Research Fellowship.

³ To whom requests for reprints should be addressed.

Received 1/27/92. Accepted 5/ 7/92.

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