Characterization of dualtropic type C retroviruses isolated from spontaneous non-T lymphomas of SJL/J(V+) mice.

Endogenous XC- viruses were isolated from non-T spontaneous lymphomas of SJL/J(v+) mice. These isolates were cloned by limiting dilution procedure and characterized for biological and immunological properties. At the electron microscope these isolates showed typical retrovirus type C morphology.

Resistance to Moloney murine sarcoma virus (M-MuSV) tumor induction is associated with natural antibody production to "endogenous" Moloney leukemia virus (M-MuLV) in BALB/Mo mice.

BALB/Mo mice are characterized by early expression of "endogenized" M-MuLV and are resistant to M-MuSV tumor induction. Furthermore, compared to normal BALB/c mice, sera from BALB/Mo mice exhibit a significant reactivity which is specific for M-MuLV when tested in a 125I-labelled Staphylococcus protein A binding assay. The possible significance of this reactivity in conferring tumor resistance is explored.

Spontaneous lymphomas in SJL/J-(v+) mice: ecotropic and dualtropic virus expression in normal and lymphomatous tissues.

Approximately 60% of inbred SJL/J-(v+) adult mice having high levels of ecotropic endogenous XC+ virus showed virus activation within the first month of life, while the others produced virus at comparable levels later on, in an attempt to correlate the time of virus activation with the incidence and latency of lymphomas, the tails of 57 1- and 2-month-old mice were tested for virus presence, and the mice were then observed for lymphoma appearance. While all 2-month-old mice expressed ecotropic virus, only 63% of the 1-month-old mice were virus-positive. However no relationship existed between early virus production (within 1 month) or late virus production and lymphoma latency, total lymphoma incidence, and histopathology.

Leukemia-cell rejection due to T-region encoded antigens.

The role of H-2- and T-region products in determining allogeneic cell rejection was evaluated in H-2 congenic and recombinant mice by transplanting A1ATH and A6ATL leukemia cell lines induced in A.TH and A.TL strains, respectively, by Moloney murine leukemia virus.

T lymphocyte tolerance and early appearance of virus-induced cell surface antigens in Moloney-murine leukemia virus neonatally injected mice.

Regression of Moloney-murine sarcoma virus- (M-MSV) induced sarcomas in normal adult mice is accompanied by generation of virus-specific cytotoxic T lymphocytes (CTL). However, when neonatal mice that were injected with Moloney-murine leukemia virus (M-MuLV carrier) were subsequently challenged as adults with M-MSV, the sarcomas did not regress nor did they generate CTL. This failure to produce CTL cannot be ascribed to nonspecific immunodepressive effects or to suppressor cell generation since M-MuLV carrier mice exhibit normal reactivity after allogeneic cell stimulation.

Lack of T-cell mediated cytotoxicity in M-MSV system depending on H-2 haplotypes.

The H-2 restriction phenomenon was evaluated with regard to the immune response to Moloney sarcoma virus (M-MSV)-induced tumours in the mouse. Using an in vitro 51Cr release assay the lytic activity of lymphocytes from M-MSV immune strains of mice, including several H-2 recombinant strains, was determined on leukaemic cell lines originally induced in mice of different strains by neonatal infection with Moloney leukaemia virus. In analogy with other experimental models, it was observed that a compatibility between effector and target cells at the K and/or D regions is generally necessary and sufficient to obtain the cytotoxic effect.

Histiocytosis 'X' of the central nervous system. Clinical and pathological report of a case with predominant cerebellar involvement.

The case is presented of a child with early manifestations of Hand-Schüller-Christian disease limited to exophthalmos, and rapid final progression towards a clinical picture dominated by intracranial hypertension and cerebellar involvement, caused by massive histiocytic infiltration of the cerebellum, combined with discrete subdural deposits of xanthomatous tissue and minor deposits in other parts of the central nervous system and other organs.

Secondary in vitro generation of cytolytic T-lymphocytes (CTL's) in the murine sarcoma virus system. Virus-specific CTL induction across the H-2 barrier.

Following in vitro stimulation of murine sarcoma virus Moloney isolate (M-MuSV)-immune spleen cells with syngeneic antigenically related Moloney leukemia cells, highly efficient cytotoxic T-lymphocytes (CTL's) were generated. The cytotoxic effect was directed only against H-2-compatible target cells bearing M-MuSV tumor-associated antigens (TAA). However, in a cold target competition assay a weak but detectable capacity to block CTL activity was also obtained when allogeneic Moloney leukemia cells were added.

Relationship between Moloney MSV tumor resistance and endogenous virogene expression in AKR mouse strain and its hybrids.

We have examined the induction of Moloney-MSV tumors in AKR and other mouse strains in relation to endogenous virus expression. All virus-free strains so far tested were tumor-susceptible, while AKR was resistant. The selectivity of MSV tumor resistance, characteristic of AKR mice, was associated with AKR virogens segregation in first backcross to MuLV-negative/MSV-susceptible mice, and in a few second backcross families.

Inhibitory effect of YC8 leukaemia cell line on in vitro lymphocyte reactivity.

Mitomycin-treated transplantable Moloney virus-induced lymphatic leukaemia cells (YC8) not only failed to stimulate normal allogeneic lymphocytes in one-way mixed leucocyte culture (MLC) but also exerted a strong inhibitory effect on the proliferative response of normal lymphocytes, in MLC and after stimulation by mitogens. Potentially inhibitory factors which could be released in the culture fluids by the YC8 cells were not found, but a YC8-derived adherent cell subpopulation was identified as being responsible for the in vitro suppression.

Genetics of murine sarcoma virus (MSV)--induced tumors in AKR mice: Evidence that late progressing and early regressing tumors are controlled by different gents.

The genetics of late appearing MSV tumors showing a progressive growth pattern in AKR mice was investigated. The late MSV tumor response in F1 hybrids depended on the genetic background of the non-AKR parent. Within the 4-month observation period following virus injection, (CBA X AKR) F1, (DBA/2 X AKR)F1, and (NIH X AKR)F1 developed progressing MSV tumors, which exhibited latency and growth behavior comparable to that seen in AKR mice, (BALB X AKR)F1, (B6 X AKR)F1, and (B10br x akr)f1 mice did not show any late MSV tumors.

Generation of cytotoxic cells in absence of blastogenesis by mouse leukemic cells in mixed cultures.

Primary virus-induced murine leukemias and transplantable leukemic cell lines, originally induced by virus, chemical or physical agents, failed to stimulate normal spleen cells differing at the H-2 complex or at Mls locus in the one-way mixed leukocyte culture. Lack of stimulation seems at least partially due to a nonspecific inhibitory effect since in a "three-party" culture system the leukemic cells interfered with the mixed leukocyte reaction (MLR) of normal allogeneic cells. Characterization of the leukemic cell populations used, according to their T or B cell origin, disclosed that in most cases T cell markers were present.

Immune reactivity in the Moloney strain of murine sarcoma virus oncogenesis: requirement of thymus-derived lymphocytes for in vivo protection.

To study the function of different lymphocyte populations in the Moloney strain of murine sarcoma virus (M-MuSV) tumorigenesis, we gave M-MuSV injections to CBA mice selectively deprived of thymus (T) lymphocytes by thymectomy, X-rradiation, and syngeneic bone marrow injection. Although no tumors appeared in the control group, 80% of the derived mice had tumors that grew progressively and ultimately killed them. In deprived mice, grafted with a syngeneic thymus (reconstituted mice) before or after an M-MuSV injection, tumors regressed or did not develop.