RESUMO
Different spleen and tumor cell factors modifying tumoral and metastatic growth were studied. Spleen cell culture supernatants (SCS) from small and large tumor-bearing mice enhanced tumor growth. After tumor surgery, tumor enhancement was only mediated by supernatants from large tumor resected mice. Tumor facilitation and angiogenic response were mediated by the same supernatants; different fractions for these two activities were characterized. T and non-T cells, depending on tumor burden, were responsible for the enhancing activity; but angiogenesis depended only on T cells. While augmentation of metastatic spread was produced by tumor antigens (soluble tumor extracts, tumor-cell supernatants, formolized tumor cells), primary tumor development was not modified by tumor-cell supernatants. Increased incidence of metastases was also mediated by SCS from tumor resected mice which had previously been inoculated with tumor antigens. Immune status of tumor-resected mice was evaluated by delayed-type hypersensitivity reaction. Tumor cell membranes enriched with cholesterol-hemisuccinate were able to increase anti-tumor immune response.
Assuntos
Adenocarcinoma/imunologia , Neoplasias Mamárias Experimentais/imunologia , Adenocarcinoma/patologia , Adenocarcinoma/secundário , Animais , Antígenos de Neoplasias/imunologia , Membrana Celular/efeitos dos fármacos , Ésteres do Colesterol/farmacologia , Linfócitos/fisiologia , Neoplasias Mamárias Experimentais/patologia , Neoplasias Mamárias Experimentais/secundário , Camundongos , Metástase Neoplásica , Baço/patologiaRESUMO
Different spleen and tumor cell factors modifying tumoral and metastatic growth were studied. Spleen cell culture supernatants (SCS) from small and large tumor-bearing mice enhanced tumor growth. After tumor surgery, tumor enhancement was only mediated by supernatants from large tumor resected mice. Tumor facilitation and angiogenic response were mediated by the same supernatants; different fractions for these two activities were characterized. T and non-T cells, depending on tumor burden, were responsible for the enhancing activity; but angiogenesis depended only on T cells. While augmentation of metastatic spread was produced by tumor antigens (soluble tumor extracts, tumor-cell supernatants, formolized tumor cells), primary tumor development was not modified by tumor-cell supernatants. Increased incidence of metastases was also mediated by SCS from tumor resected mice which had previously been inoculated with tumor antigens. Immune status of tumor-resected mice was evaluated by delayed-type hypersensitivity reaction. Tumor cell membranes enriched with cholesterol-hemisuccinate were able to increase anti-tumor immune response.
RESUMO
Supernatants obtained from short-cultured spleen cells (SCS) from BALB/c mice bearing a syngeneic mammary transplanted tumor--S13--showed enhancing activity on tumor growth when inoculated into the foot pad of normal syngeneic mice 24 hr before injection of S13 tumor cells. The present work was designed to characterize the spleen cell population responsible for the releasing of the enhancing factor (EF) as long as the tumor grows (small tumor bearing mice--STBM--and large tumor bearing mice--LTBM). Pretreatment of spleen cells with anti-Thy 1.2 serum + C' and nylon-wool columns were utilized to separate cell populations and to characterize the cellular source of the enhancing activity in the spleens of STBM and LTBM. In this tumor system, evidence is presented for distinct enhancing cell population operating in the spleens of STBM and LTBM. In early stages of tumor development, the EF was found to be associated with T and non-T cells, whereas in advanced stages of tumor growth, this activity was found to be associated with only T cells.