Peripheral blood lymphocytes and EAC-rosette forming cells in B77 tumor bearing rats.

The percentage and absolute numbers of peripheral blood lymphocytes and EAC-rosette forming cells were evaluated in B77 tumor bearing rats. The peripheral blood lymphocytes were in high level even in rats bearing very small tumors; this result suggest the mobilization of lymphoyctes into peripheral blood in tumor bearing rats. The increase of EAC-rosette forming cells was accompanied with the growth of tumors.

The leukocyte response of Japanese quail to Rous sarcoma virus-induced tumors.

In male Japanese quail, different circulating leukocyte responses were observed for progressors (birds developing a massive tumor that persisted throughout the experiment) and regressors (birds developing a tumor that gradually disappeared) after initial challenge with Rous sarcoma virus (RSV). Blood was sampled before and at weekly intervals postinoculation. Blood smears were prepared and stained with Diff Quik, and a light microscope (1000 x) was used in a direct count of 50 fields. Leukocytes were classified as heterophils, lymphocytes, monocytes, or eosinophils. The significant increase (P < 0.05) in total leukocytes at 14 days in regressors and progressors was consistent with the increase in tumor growth. The regressors' individual percentage of leukocytes did not deviate from control values, whereas the progressors' percentages of heterophils and monocytes were significantly higher (P < 0.05) and of lymphocytes significantly lower (P < 0.05) than those of controls by 14 days postinoculation. Indicative of this was the progressors' heterophil to lymphocyte ratio, which was significantly higher (P < 0.05) than that of controls 14 days post RSV challenge and remained elevated throughout the experiment. These findings suggest that the progressors' immune response is suppressed by proliferation of malignant cells. Therefore, the heterophil to lymphocyte ratio may be used in addition to tumor size to identify those birds that will regress RSV-induced tumors.

Protein concentrations and immunosuppressive properties of serum in chickens experimentally infected with avian tumor viruses.

Sera from chickens affected by Marek's disease or developing Rous sarcoma were investigated. There were changes in the protein fractions, and the amount of alpha and beta fractions was consistently increased. At the same time, immunosuppressive factors were found to inhibit the number of plaque-forming cells in the spleen of mice immunized with sheep red blood cells.

In vivo effect of three transformation-defective mutants of subgroup C avian sarcoma viruses.

Three transformation-defective mutants derived from avian sarcoma viruses of subgroup C, td PR-RSV-C (Vogt), td B77 (Toyoshima) and td daPR-RSV-C (isolated in our laboratory), were injected intravenously into 12-day-old chicken embryos and intraperitoneally into newly-hatched chickens. Both Brown Leghorn chickens and F1 hybrids of two inbred chicken lines (C X I) were used. Haematological changes and formation of visible tumours were evaluated in animals kept for 8-9 months. All three td mutants produced in a significant proportion of intraembryonally injected animals haematological disorders which, in certain cases, resembled the anaemic and proliferative type of erythroblastosis. Most conspicuous symptoms of erythroblastosis were seen after td daPR-RSV-C which also gave rise to two sarcomas, containing transforming viruses. The possible character of oncogenic information retained or acquired by the TD mutants is discussed.

Haematological and pathomorphological studies on chickens inoculated with transformation-defective sarcoma virus.

A transformation-defective mutant of Rous sarcoma virus (td PR-RSV-C) inoculated into chicken embryos caused a number of pathological changes in chickens after hatching. Disturbances in haematopoiesis were manifested by anaemia of different degree and by the presence of immature blood elements in the peripheral blood. The haematological picture of erythroblastosis was confirmed histologically. In addition to erythroblastosis, lymphoid leukosis and a proliferative lymphosarcoma-like tumour were demonstrated histologically.

Activation of complement in quails bearing Rous sarcoma virus-induced tumors.

The concentration of serum C3 in quails bearing tumors induced by Rous sarcoma virus (RSV) was elevated in parallel with tumor growth, whereas serum C3 levels in quails inoculated with avian leukosis virus, which lacks transforming activity, showed a pattern similar to that in mock-infected quails. C3 deposition was also observed in almost all tumor cells at the tumor developing stage. These findings obtained in vivo suggest that the cells transformed by RSV activated the C3 on their surfaces.

Tumour-associated transplantation antigen in sera of rats with large RSV-induced sarcomas.

A factor inhibiting tumour growth in syngeneic hosts was found in the sera of inbred Lewis rats carrying Rous sarcoma virus-induced tumour (RSL). The findings presented here suggest that the serum factor is a tumour-associated transplantation antigen (TATA) shed from the neoplasm into the circulation. All the tumour bearers' sera tested with RSL cells were negative in indirect membrane immunofluorescence;however, on passive transfer into syngeneic rats, they protected the animals against the growth of an RSL tumour inoculum. A similar protective effect was also observed after injection of TATA prepared from RSL cell membranes by solubilization with potassium cholate. When incorporated into Freund's adjuvant, tumour-bearers' sera immunized the animals against a subsequent RSL sarcoma graft. Sera collected from immunosuppressed rats bearing large sarcomas which presumably contain neither tumour-specific antibody nor antigen-antibody complexes, transferred inhibition of tumour growth to syngeneic hosts. Intact immunological reactivity of recipients was a necessary prerequisite for the protective effect of sera, since the passive transfer of an inhibitory serum to immunosuppressed rats did not inhibit tumour growth. We assume that the TATA present in tumour-bearers' serum is released from the growing neoplasm as a result of either cell death or membrane metabolic turnover.