Expression of major histocompatibility antigens and leucocyte infiltration in benign and malignant human breast disease.

The reactivity of murine monoclonal antibodies (McAbs) directed against the monomorphic determinants of Class I and Class II antigens of the major histocompatibility complex (MHC), and against antigens expressed by discrete populations of leucocytes was studied using the indirect immunoperoxidase technique on serial tissue sections of 16 benign and 17 malignant primary human breast tumours. Class I antigens (detected by the McAb 2A1) were consistently associated with stromal leucocytes, fibroblasts and vascular endothelium, but expression on epithelial cells particularly of malignant provenance, was more variable. Class II antigens (detected by TDR 31.1) were present upon a variety of cell types which also included sporadic expression on malignant and benign epithelia. The distribution of leucocytes grossly monitored with 2D1 (reactive with a common leucocyte antigen) was largely interepithelial and periductal in benign lesions. Leucocytes were generally more numerous in malignant tumours, where they were largely confined to the stroma. The majority (approximately 75%) of leucocytes were T lymphocytes (reactive with UCHT1), some of which appeared to react with TDR 31.1 and were therefore activated. Ratios of helper/inducer (OKT4+) and suppressor/cytotoxic (OKT8+) subsets generally exceeded unity in malignant neoplasms. There was no correlation between the extent and distribution of T cells and the HLA status of the epithelial cells. Leucocytes detected by the monoclonal antibody OKM1 which reacts with monocytes/macrophages, granulocytes and large granular lymphocytes were numerically few and again mainly confined to the stroma. In a limited number of tests, leucocytes detected with HNKl, reactive with a differentiation antigen expressed on some cells which mediate natural and antibody-dependent cellular cytotoxicity in vitro although detectable interepithelially in benign tumours, were virtually absent from malignant tissue. HNK1 also cross-reacted with myoepithelial cells in the ducts of benign lesions.