“Concomitant immunity” in murine tumours of non-detectable immunogenicity

Abstract

Summary Various immunization assays were used to demonstrate the lack of immunogenicity of three BALB/c tumours of spontaneous origin and of a fourth one resulting from foreign body tumorigenesis. All four tumours inhibited the growth of a second implant of the same tumour into the contralateral flank. In our tumour models "concomitant immunity" (1) was not mediated by macrophage or T-cell dependent immune reactions: both thymectomized BALB/c and nude mice (treated or untreated with silica) gave the same results as intact mice; (2) showed some degree of non-specificity, inhibiting the growth of a different tumour in 3/4 cases; though, the existence of a specific component could not be discarded; (3) was proportional to the volume of the primary tumour at the time of the second challenge; (4) was dependent on actively growing primary tumour, not being obtained with progressively increasing daily inocula of irradiated tumour cells; (5) was detectable in an actively growing secondary tumour: recurrent growth after partial surgical excision was inhibited and (6) involved cytostasis of the secondary tumour: a syngeneic graft of the overlying skin led to tumour growth while histological studies revealed the presence of viable tumour cells. It is postulated that "concomitant immunity" or resistance can be generated without the active participation of the immune system and that tumour-related factors are, in certain cases, responsible for blocking the growth of secondary tumours.

A serum-mediated mechanism for concomitant resistance shared by immunogenic and non-immunogenic murine tumours

“…In effect, concomitant resistance induced by strongly immunogenic tumours has been described as tumour specific and mainly mediated by T-cell-dependent cytotoxic mechanisms, not different from a classical immunological rejection (Belehradek et al, 1972;Chandradasa, 1973;Tuttle et al, 1983;North, 1984;Akporiaye et al, 1988). On the other hand, concomitant resistance induced by weakly or non-immunogenic tumours has been described as non-specific and mediated by a cytostatic mechanism presumably unrelated to any known conventional immunological mechanism (Gorelik et al, 1981;Gorelik, 1983;Ruggiero et al, 1985;Meiss et al, 1986;Bonfil et al, 1988). In a former paper (Ruggiero et al, 1990) we demonstrated that the serum from mice bearing non-immunogenic tumours exhibited a growth-inhibitory activity (not attributable to cytotoxic antibodies) on in vitro proliferation of tumour cells that was proportional to the intensity of concomitant resistance.…”

“…It was maintained by s.c. serial passages in syngeneic mice and was used between passages 69 and 170. More detailed description of this tumour is given elsewhere (Ruggiero et al, 1985;Zahalka et al, 1993).…”

Enhancement of anti-tumour immunity in syngeneic mice after MHC class II gene transfection

“…Tumour LB is a T-cell leukaemia, which spontaneously arose in a BALB/c mouse and has been maintained by serial passages in the peritoneal cavity of syngeneic hosts (Ruggiero et al, 1984;Alvarez et al, 1989;Lugasi et al, 1990). LBC is an established cell line derived from LB leukaemia (Mongini et al, 1991).…”

“…In previous work we have reported the establishment and characterisation of the LBC cell line (Mongini et al, 1991) derived from the original T-cell leukaemia LB (Ruggiero et al, 1984). LBC cells express the following surface markers: Thy-1, Lyt-2 (CD 8), CD 41ow+ CD 25 (IL-2 receptor, a chain), class I (Kd and Dd), but not class II (I-Ad, I-Ed) gene products.…”

Anti-inflammation induced by counter-irritation or by treatment with non-steroidal agents inhibits the growth of a tumour of non-detected immunogenicity

“…The T-helper cell leukaemia (LB), which arose spontaneously in a 6-month-old Balb/c male mouse (Ruggiero et al, 1985) was, at the beginning of this study, in its 58th s. …”