The immunological basis of endotoxin-induced tumor regression. Requirement for a pre-existing state of concomitant anti-tumor immunity

It was shown that of four syngeneic, murine tumors investigated, only those that evoked the generation of a state of concomitant anti-tumor immunity were susceptible to endotoxin-induced regression. Moreover, the temporal relationship between the generation of concomitant immunity and the onset of s...

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Bibliographic Details
Published inThe Journal of experimental medicine Vol. 148; no. 6; pp. 1560 - 1569
Main Authors Berendt, M J, North, R J, Kirstein, D P
Format Journal Article
LanguageEnglish
Published United States The Rockefeller University Press 01.12.1978
Subjects
Animals
Endotoxins - pharmacology
Endotoxins - therapeutic use
Fibrosarcoma - immunology
Immunity - drug effects
Immunotherapy
Mammary Neoplasms, Experimental - immunology
Mice
Neoplasms, Experimental - immunology
Neoplasms, Experimental - therapy
Sarcoma, Experimental - immunology
Stimulation, Chemical
T-Lymphocytes - immunology
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Summary:It was shown that of four syngeneic, murine tumors investigated, only those that evoked the generation of a state of concomitant anti-tumor immunity were susceptible to endotoxin-induced regression. Moreover, the temporal relationship between the generation of concomitant immunity and the onset of susceptibility to endotoxin-induced regression points to the likely possibility that tumor regression depends on the preceding acquisition of the specifically-sensitized, effector T cells that express concomitant immunity. It is suggested that endotoxin-induced hemorrhagic necrosis which invariably precedes tumor regression serves to create conditions inside the tumor that are conducive to the entry and the functioning of effector T cells. It is also suggested that tumor necrosis factor causes hemorrhagic necrosis rather than tumor regression.
Bibliography:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
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ISSN:0022-1007
1540-9538
DOI:10.1084/jem.148.6.1560