Immunity to Infection, Allograft Immunity and Tumour Immunity: Parallels and Contrasts

Nelson, D. S.

doi:10.1111/j.1600-065x.1974.tb00134.x

Cited by 18 publications

(22 citation statements)

References 166 publications

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“…Cross-protection against unrelated micro-organisms and against tumour growth results from infection with intracellular bacterial and protozoan parasites (North, 1974;Bast, Bast and Zbar, 1976;Nelson, 1974). This paper reports part of a study of the anti-tumour effects itiduced by one such organism, the attenuated llRX strain of Salmonella enteritidis (Hardy and Kotlarski, 1971;Ashley, Kotlarski and Hardy, 1974).…”

Section: Introductionmentioning

confidence: 99%

IN VITRO AND IN VIVO CYTOTOXICITY INDUCED BY AN ATTENUATED SALMONELLA: RELATION TO BACTERIAL CARRIER STATE AND RESISTANCE TO TUMOUR GROWTH

Ashley

Kotlarski

1982

Aust J Exp Biol Med

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Summary In vivo and in vitro parameters of tumour resistance were examined after immunization of mice with the attenuated 11RX strain of S. enteritidis. During the bacterial carrier state produced by intraperitoneal (i.p.) or intravenous (i.v.) injection of 11RX the mice were resistant to i.p. tumour growth, could destroy i.p. injected 125I‐ or 131I‐labelled tumour cells in vivo and had non‐specifically cytotoxic peritoneal cells (PC) which could lyse 51Cr‐labelled tumour cells in vitro. Most of the in vivo and in vitro cytotoxic activity could be attributed to activated macrophages (La Posta et al., 1982). The predominantly local nature of 11RX‐induced anti‐tumour activity was indicated by the superiority of the i.p. route of infection for induction of tumour resistance and in vivo and in vitro cytotoxicity. After i.v. injection of 11RX, none of the anti‐tumour effects outlasted the bacterial carrier state. However, after i.p. infection, a dichotomy was observed between in vitro and in vivo anti‐tumour effects. In vitro PC cytotoxicity lasted only for the length of the 11RX carrier state (approximately 30 days), whereas resistance to i.p. tumour growth lasted for 60 to 100 days and was correlated closely with cytotoxic activity measured in vivo. Possible reasons for this dichotomy are discussed.

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Section: Introductionmentioning

confidence: 99%

IN VITRO AND IN VIVO CYTOTOXICITY INDUCED BY AN ATTENUATED SALMONELLA: RELATION TO BACTERIAL CARRIER STATE AND RESISTANCE TO TUMOUR GROWTH

Ashley

Kotlarski

1982

Aust J Exp Biol Med

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“…The tumours were designated C-1, C-4 and C-9 of CBA/J mice, A-1 of A/J mice and H-1 of CBA/H mice. All the tumours except C-1 induced concomitant immunity; only C-1 metastasized Nelson, 1974;Kearney et al, 1975 Sections 5 ,um thick were stained with haematoxylin and eosin. All tumours were characterized as inducing or failing to induce concomitant immunity on the basis of the fate of footpad challenge injections 14 days after primary s.c. tumour isografts .…”

Section: Methodsmentioning

confidence: 99%

Macrophages and lymphoid tissues in mice with concomitant tumour immunity

Nelson¹,

Kearney²

1976

Br J Cancer

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Summary.-The growth in mice of subcutaneous isografts of any of 5 methylcholanthrene-induced fibrosarcomas was associated with macrophage stimulation, reflected in an increased incidence of DNA-synthesizing cells among macrophages in the uninjected peritoneal cavity. This occurred at some stage with 4 tumours that induced concomitant immunity and one that did not. Some degree of splenomegaly also occurred with all 5 tumours. The spleens of all the tumour-bearing mice showed histological evidence of increased haemopoietic activity. Histological changes in the lymphoid elements of the spleen were very different with different tumours, ranging from lymphoid stimulation to lymphoid atrophy. The lymph nodes draining the sites of primary isografts which induced concomitant immunity showed signs of stimulation in the paracortical areas, followed by plasmacytopoiesis in the medullary areas. Stimulation of the paracortical areas was not detected in the nodes draining sites of injection of a tumour not inducing concomitant immunity. Nodes draining the sites of challenge isografts in mice exhibiting concomitant immunity showed plasmacytopoiesis.

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“…The time of death from growth of the primary tumour varies widely with the tumour as well as the size of the inoculum; a subcvitaiaeows iBOCMlum ot W' eells normally will kill the host within 28-45 days. Concomitant immunity is thymus-dependent, but there is evidenee that different effeetor mechanisms may be operating during the speeifie and non-specific phases (Nelson, 1974;Kearney, Basten and Nelson, 1975;North and Kirstein, 1977). It was therefore of interest to examine the effeets on natural resistanee and on speeifie and non-speeific concomitant immunity to these tumours of agents reputedly affeeting maerophages and/or DTH; siliea, earrageenan, irradiation, niridazole and reserpine.…”

Section: Introductionmentioning

confidence: 99%

Macrophages and Resistance to Tumours

Nelson

1978

Aust J Exp Biol Med

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Summary Early, specific concomitant immunity to each of four tumours was inhibited by treatment with silica or carrageenan. Late, non‐specific concomitant immunity was, with one exception, not inhibited by these agents. Treatment of non‐immune mice with silica at certain critical periods before challenge promoted the growth of four of six syngeneic methylcholanthrene‐induced tumours in their feet. Treatment with carrageenan was much less effective. Early and late concomitant immunity were inhibited by one or more agents inhibiting delayed‐type hypersensitivity: irradiation, niridazole and reserpine. Irradiation of nonimmune mice did not effect the growth of tumours in their feet. Treatment of non‐immune mice with niridazole or reserpine actually inhibited the growth of some tumours. It is suggested that (a) mice offer some natural resistance to tumour growth, macrophages perhaps being effectors; (b) some tumour isografts may survive only if an inflammatory reaction occurs; (c) mechanisms akin to those of delayed‐ type hypersensitivity operate in the expression of concomitant immunity; (d) macrophages are important in early, specific concomitant immunity, but perhaps less so in the late non‐specific phase.

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Immunity to Infection, Allograft Immunity and Tumour Immunity: Parallels and Contrasts

Cited by 18 publications

References 166 publications

IN VITRO AND IN VIVO CYTOTOXICITY INDUCED BY AN ATTENUATED SALMONELLA: RELATION TO BACTERIAL CARRIER STATE AND RESISTANCE TO TUMOUR GROWTH

IN VITRO AND IN VIVO CYTOTOXICITY INDUCED BY AN ATTENUATED SALMONELLA: RELATION TO BACTERIAL CARRIER STATE AND RESISTANCE TO TUMOUR GROWTH

Macrophages and lymphoid tissues in mice with concomitant tumour immunity

Macrophages and Resistance to Tumours

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