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Войти в исследования The Journal of dermatologic surgery and oncology · 1993
Suppression of the delayed type hypersensitivity response by tumor facilitating factor of B16 melanoma. A tumor factor suppresses immune responses.
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Burnstein P, Brody N I
Аннотация
BACKGROUND: Tumor facilitating factor is a cell surface glycoprotein produced by B16 melanoma that has been found to reduce the lethal inoculum for B16. Tumor facilitating factor induces macrophage spreading in vitro, reduces macrophage chemotaxis in vivo, and depresses lymphocyte mitogenesis in vitro.
OBJECTIVE: It is assumed that the immune modifying effects are responsible for tumor facilitation. As tumors may be poor immunogens or inducers of inflammation, studies were conducted to determine whether tumor facilitating factor alters the inflammatory cascade of cells found in infiltrates of delayed type hypersensitivity.
RESULTS: Freeze-thawed B16 cells, used as the source of TFF, caused a suppression of delayed type hypersensitivity measured as ear swelling in the mouse. When culture supernatant was substituted for freeze-thawed cells as a source of TFF and injected at different time points of the delayed type hypersensitivity response, the greater suppression was with tumor facilitating factor injections at 24 hours pre-elicitation only (82%), and 24 hours both presensitization and pre-elicitation (89%). Immunohistological staining demonstrated that tumor facilitating factor decreases ear thickness and cellular infiltrates, specifically Mac-1 staining cells, to a site of delayed hypersensitivity. Peritoneal cell analysis confirmed these findings.
CONCLUSION: These data are consistent with the hypothesis that tumor facilitating factor alters immune functions including macrophage and lymphocyte mobility and recruitment to a target site, thereby allowing for facilitation of tumor growth.
OBJECTIVE: It is assumed that the immune modifying effects are responsible for tumor facilitation. As tumors may be poor immunogens or inducers of inflammation, studies were conducted to determine whether tumor facilitating factor alters the inflammatory cascade of cells found in infiltrates of delayed type hypersensitivity.
RESULTS: Freeze-thawed B16 cells, used as the source of TFF, caused a suppression of delayed type hypersensitivity measured as ear swelling in the mouse. When culture supernatant was substituted for freeze-thawed cells as a source of TFF and injected at different time points of the delayed type hypersensitivity response, the greater suppression was with tumor facilitating factor injections at 24 hours pre-elicitation only (82%), and 24 hours both presensitization and pre-elicitation (89%). Immunohistological staining demonstrated that tumor facilitating factor decreases ear thickness and cellular infiltrates, specifically Mac-1 staining cells, to a site of delayed hypersensitivity. Peritoneal cell analysis confirmed these findings.
CONCLUSION: These data are consistent with the hypothesis that tumor facilitating factor alters immune functions including macrophage and lymphocyte mobility and recruitment to a target site, thereby allowing for facilitation of tumor growth.