INFILTRATION OF MONONUCLEAR INFLAMMATORY CELLS INTO PRIMARY COLORECTAL CARCINOMAS - AN IMMUNOHISTOLOGICAL ANALYSIS

Local immunoregulation mediated by mononuclear tumour-infiltrating cel ls is considered of importance for tumour progression of colorectal ca ncer, although the balance between immunosuppressor and cytotoxic acti vities is unclear. Colorectal cancers from 26 patients were investigat ed using a panel of monoclonal antibodies in order to identify subsets of mononuclear inflammatory cells and to study their pattern of distr ibution in relation to tumour stage and cytotoxic immune reactivity ag ainst the tumour. In all but five tumours, mononuclear cells, lymphocy tes or monocytes were present in fairly large numbers, particularly in the stroma. The infiltration of CD4(+) mononuclear cells predominated over the CD8(+) subset. Infiltration near the tumour cells was found in four cancers only. Stromal infiltration of CD11c(+) macrophages was found in all but eight rumours. Small regressive areas, in which the histological architecture of the tumours was broken down, were found i n 17 rumours with intense or moderate infiltration by CD4(+) lymphocyt es or CD11c(+) macrophages. Probably this destruction of tumour tissue was caused by cytotoxic activity of the tumour-infiltrating mononucle ar cells. In Dukes' class A and B tumours, CD4(+) lymphocytes predomin ated over CD4(+) cells with macrophage morphology, but the latter were increasingly found in Dukes' class C and D disease, The occurrence of MHC It-positive macrophages and lymphocytes in different Dukes' class es was similar to that of CD4 cells. In contrast to this, CD11c(+) and CD11a(+) cells were more frequent in Dukes' A and B class tumours com pared with Dukes' C and D, Four out of nine rumours of the latter stag es showed a poor inflammatory reaction. The interpretation of our resu lts is that the subsets of tumour-infiltrating mononuclear cells chang e with advancing Dukes' class and that the local immune control is gra dually broken down in progressive tumour growth, even if some cytotoxi c activity is still present.