| pubmed-article:3552955 | pubmed:abstractText | Monoclonal antibodies and the avidin-biotin immunoperoxidase technique were used to study the expression of major histocompatibility complex antigens and the nature of the inflammatory cell infiltrate in 10 testicular seminomas. Tumor cells did not react with anti-HLA-A,B,C, anti-HLA-DR, anti-HLA-DQ, and anti-beta 2 microglobulin antibodies to major histocompatibility antigens. All of the 10 tumors contained a slight to marked inflammatory cell infiltrate at the periphery of the tumor, in the connective tissue septa, and in the tumor lobules. The lymphocytes were predominantly T cells; B lymphocytes were rare. The tissue available for study from seven tumors showed tumor lobules separated by delicate fibrovascular septa; T lymphocytes with a cytotoxic-suppressor phenotype predominated in this area in six tumors. In the four tumors in which peripheral tissue was available for study, cells with a helper-inducer phenotype predominated at the tumor margin. Tissue from three tumors showed stromal sclerosis and a dense lymphohistiocytic infiltrate separating individual and small nests of tumor cells; T cells with a helper-inducer phenotype predominated in these cases. Aggregates of macrophages that expressed OKM-1 and Leu-M3 were present in eight of 10 tumors. These findings indicate that two types of immune reactions may be operating: a delayed-type hypersensitivity response at the periphery and a cytotoxic-suppressor effector mechanism in the tumor lobules. Furthermore, major histocompatibility complex antigens are not involved in eliciting the inflammatory response. | lld:pubmed |
