THE CANCER PROCESS AS A TYPE OF IMMUNOCOMPLEX HYPERSENSIBILITY INVOLVING C3B, NATURAL-KILLER CYTOTOXICITY AND ANTIBODY-DEPENDENT CELL CYTOTOXICITY - PROPOSALS FOR TUMOR-IMMUNOTHERAPY AND VACCINE

I have previously assumed that stem tumour cells are 'para-embryonal c ells' (PECs) poor or missing in major histocompatibility complex (MHC) antigens. PECs might induce adjoining differentiated hyperplastic cel ls to also express tumoral phenotype and properties, thus transforming them into 'differentiated para-embryonal cells' (DPECs), MHC-endowed. In such a way, PECs, MHC-lacking, would be automatically surrounded b y DPECs, MHC-endowed: this tumour organization was experimentally foun d by Cordon-Cardo et al in a variety of cancers. Now, I suggest that s uch a tumour histology might preferentially induce an anti-DPEC T cell immune response which, sparing PECs, might release increasing amounts of DPEC antigens in the peritumour site. DPEC antigens might increase synthesis of specific antibodies and subsequent immunocomplex formati on at the peritumour site. Here, abundant immunocomplexes might react th rough their Fc pieces with CD16 receptors of antibody-dependent cel l cytotoxicity (ADCC)-endowed immune cells (natural killer (NK) cells, macrophages, polymorphonuclear cells). These cells would thus be stim ulated to secrete their lytic factors before and without their coming into contact with target tumour cells. On the other hand, abundant imm unocomplexes at the peritumour site might massively activate the compl ement system, thus generating large amounts of C3b. C3b might react wi th CD11b receptors of NK cells, stimulating them to also secrete their lytic factors in an ectopic way at the peritumour site, thus impairin g NK cytotoxicity. In such a way, in the absence of ADCC and NK cytoto xicity, a tumour cell enhancement might easily occur. In the light of these ideas, a strategy for antitumour immunotherapy and vaccine is th en proposed.