Resistance to a non-immunogenic tumor, induced by Corynebacterium parvum or Listeria monocytogenes, is abrogated by anti-interferon gamma.
The complex processes that determine the outcome of the interaction of tumor and host were explored in the operationally simple and reproducible rat D-12 ascites tumor model. Animals exhibit weak spontaneous resistance against this tumor that is not augmented by repeated inoculation, by various routes, of irradiated syngeneic D-12 tumor cells, but considerably enhanced after local administration of heat-killed Corynebacterium parvum (CP) or Listeria monocytogenes (LM) organisms. Inoculation of conventional or monoclonal anti-rat IFN gamma antibodies into the same compartment did not affect spontaneous tumor resistance, but largely abrogated the tumor-protective effect triggered by CP or LM. Our findings support the concept that IFN gamma, produced by T cells in the course of the specific immune response raised against immunogenic micro-organisms, is able to enhance and to maintain local tumor resistance and thus to strengthen the capacity of the host to cope with a non-immunogenic tumor.
Keller
R
R
Immunobiology Research Group, University of Zurich, Switzerland.
Keist
R
R
Leist
T P
TP
van der Meide
P H
PH
D000818:Animals; D002286:Carcinoma, Ehrlich Tumor / Q000276:immunology*; D004195:Disease Models, Animal; D016233:Immunotherapy, Active; D007371:Interferon-gamma / Q000276:immunology*; D008087:Listeria / Q000276:immunology*; D011425:Propionibacterium acnes / Q000276:immunology*; D051381:Rats; D011919:Rats, Inbred Strains
D007371:Interferon-gamma