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K J Blank

Publications and source records attributed to K J Blank.

At least 55 records · Page 3Linked to original sources
PubMed1986

Antigenic changes in gp70 associated with the adult variant of Gross murine leukemia virus, WB91.

Gross murine leukemia virus (GV) is not leukemogenic in adult mice whereas a variant of GV, WB91, is highly leukemogenic regardless of the age of the inoculated animal. FACS and SDS-PAGE analysis have demonstrated that these viruses differ at least with respect to the env-encoded gp70 molecule. FACS analysis of virus infected or virus transformed cells with a type specific monoclonal antibody (mAb #55) indicated a difference in determinants associated with gp70 expressed by the two viruses. Rat antisera raised against GV- or WB91-induced tumor cells demonstrated that there were no crossreactive determinants between the gp70 molecules expressed on these tumor cells as recognized by the rat antisera. This difference in the gp70 molecules encoded by WB91 and GV may account for the ability of the WB91 virus to induce leukemia in adult mice, possibly by affecting the immunogenicity of the virus.

AKR murine leukemia virus↗
PubMed1986

Evidence for H-2-linked control of retrovirus production in Friend virus-induced tumor cell lines.

In Friend leukemia virus-induced tumor cell lines derived from mice congenic with respect to the H-2 complex, most cell lines expressing the H-2k haplotype continuously produced infectious exogenous virus in culture, whereas most cell lines expressing the H-2b or H-2d haplotype stopped producing virus during in vitro passage. This apparent H-2-linked control of virus production did not appear to be the result of alteration of the provirus or resistance to superinfection. The implications of this finding with respect to virus-induced leukemogenesis are discussed.

Animals↗
PubMed1985

Poly I:C or IFN-alpha/beta treatment inhibits macrophage induced T cell proliferation.

IFN-alpha/beta has been previously shown to cause the suppression of various immune responses. The reason for this immunosuppression, however, remains unknown. The studies described in this report demonstrate that treatment of mice with poly I:C or partially purified IFN alpha/beta inhibited the ability of KLH pulsed macrophages to induce proliferation of KLH immune T cells. This failure to generate antigen induced proliferation was not caused by the production of prostaglandins or other suppressive molecules by IFN treated macrophages, nor did this treatment induce suppressor macrophages.

Animals↗
PubMed1984

Variation in p30-related proteins in gross virus-induced tumor cell lines derived from H-2 congenic mice.

p30-related proteins were examined in three in vitro--passaged Gross virus--induced cell lines derived from mice congenic at the H-2 complex: BALB.K-gv-1 (H-2k) (BkGV1), which produces infectious, oncogenic virus, and BALB.B-gv-1 (H-2b) (BbGV1) and BALB/c-gv-1 (H-2d) (BdGV1), which stopped producing infectious virus early in their passage history. The producer BkGV1 line made p30 and its expected precursors. BbGV1 and BdGV1 cells had multiple changes in p30-related protein expression. BbGV1 cells (i) synthesized a truncated gag precursor polyprotein of ca. 47 kilodaltons, (ii) expressed fewer p30-related molecules per cell on their surface than BkGV1 cells, (iii) produced functional reverse transcriptase, and (iv) budded morphologically mature virions which were neither infectious nor oncogenic. BdGV1 cells (i) produced no p30 but expressed some high-molecular-weight proteins with p30 determinants, (ii) expressed fewer p30-related determinants on their surface than BbGV1 cells, and (iii) harbored immature intracisternal viral particles (type A) but did not exhibit budding virions.

AKR murine leukemia virus↗
PubMed1983

Identification of a variant of gross leukemia virus that induces disease in mice inoculated as adults.

Gross murine leukemia virus normally induces leukemia (thymic lymphoma) in mice inoculated as neonates, but not as adults. We have isolated an apparent variant of this virus which induces thymomas when inoculated i.p. into susceptible adult mice. Using H-2 congenic BALB and C57BL mice, susceptibility to virus-induced thymomagenesis was found to be linked to the H-2 complex. In addition, a radioresistant immune mechanism leading to inhibition of tumor growth was observed in mice with a C57BL but not a BALB background.

AKR murine leukemia virus↗
PubMed1983

Effect of interferon on thoracic duct lymphocyte output: induction with either poly I:poly C or vaccinia virus.

Systemic inoculation of the interferon (IFN) inducer polyinosinic-polycytidylic polyribonucleotide (poly I:poly C) into CBA/J mice produces a significant decrease in the number of thoracic duct lymphocytes (TDL) collected 6 to 22 hr after injection. The number of TDL is restored to normal levels by 48 to 64 hr. Residual TDL collected during the inhibition period of poly I:poly C treatment showed a phenotypic profile similar to phosphate-buffered saline- (PBS) treated control groups when examined for Lyt-1.1, Lyt-2, Thy-1.2 and Iak surface markers. Interferon is implicated as the mediator of this phenomenon since: 1) Inoculation of exogenous IFN can induce a similar suppression in the number of recoverable TDL. 2) Pretreatment of mice with sheep anti-murine IFN serum can block this effect of poly I:poly C. Similar experiments with vaccinia virus demonstrate that although live virus can partially suppress the TDL output, almost complete suppression is achieved with ultraviolet (UV)-inactivated virus. Vaccinia virus-induced suppression of the number of TDL also appears to be caused by IFN since: 1) UV-inactivated virus induces significantly higher serum levels of IFN in comparison to live virus. 2) The suppression of TDL output by either live or UV-inactivated vaccinia virus can be blocked by pretreatment with anti-murine IFN. These findings suggest that the immunosuppression often associated with viral infections may be at least partially due to a decrease in lymphocyte recirculation mediated by the IFN initially released in response to the virus.

Animals↗
PubMed1982

Use of H-2:H-7 congenic mice to study H-2-mediated resistance to Friend leukemia virus.

Congenic and double congenic mice expressing different H-7 alleles with varying H-2 haplotypes on the C57BL/10 (B10) background were tested for their susceptibility to Friend virus (FV) infection. Mice expressing the H-7b allele derived from BALB/c were susceptible to FV infection whereas mice expressing the H-7a allele of B10 were absolutely resistant. Coexpression of H-7b and the H-2a and H-2d haplotypes determined high susceptibility; mice expressing both H-7b and H-2b were relatively resistant compared to H-7b mice expressing H-2a or H-2d. Parallel experiments with BALB/c and BALB.B recipients did not demonstrate differences in susceptibility associated with H-2d and H-2b. Mapping experiments with the H-2h4 and H-2i5 recombinants indicated that the gene determining relative resistance to FV-induced spleen focus formation mapped to the K-end (KbAb) of H-2b. Female recipients expressing H-7b, regardless of their H-2 haplotype, were more susceptible to FV infection than their syngeneic male counterparts. These experiments demonstrate the utility of congenic and double congenic strains that define H-7 and Fv-2 on different H-2 haplotype backgrounds for the analysis of Fv-2:H-7:H-2 interactions in determining susceptibility to FV infection.

Animals↗
PubMed1981

Effect of anti-interferon serum on Friend virus infection and Fv-1-mediated resistance.

The purpose of these studies was (1) the quantitation of the protective effect of endogenous interferon (IFN) in the Friend virus (FV) system, and (2) the determination of the role of IFN in the relative resistance to FV mediated by the Fv-1-gene. In these studies, mice from two strains differing with respect to their Fv-1 alleles were treated with sheep anti-mouse IFN serum immediately prior to infection with N-tropic FV. The effect of this pretreatment showed that the neutralization of FV-induced IFN by anti-IFN resulted in a two to tenfold increase in susceptibility to FV infection as measured by the appearance of macroscopic foci of erythroleukemic cells on the splenic surface as compared to control mice which received normal sheep serum. At higher virus doses, an increase in spleen weight in anti-IFN-treated mice was also observed. Mice resistant to FV by virtue of their Fv-1 allele were affected by anti-IFN pretreatment only as much as mice from the susceptible strain. Therefore, IFN appeared to play no role in Fv-1-mediated resistance.

Animals↗
PubMed1980

Evidence that endogenous ecotropic virus is not expressed in AKR thymic lymphoid cells of chimeric hosts.

AKR/J thymocytes derived from fetal liver cells do not produce virus when they differentiate in lethally irradiated B10.K mice, whereas spleen and bone marrow cells are virus producers. In contrast, B10.K thymocytes that differentiate in lethally irradiated AKR mice become virus producers. These results suggest that infection of the thymus in AKR mice is initiated in thymic stromal cells.

Animals↗
PubMed1980

Induction of interferon in AKR mice by murine leukaemia viruses.

A high percentage of AKR mice develop spontaneous leukaemia which has shown to be associated with the early expression of ecotropic murine leukaemia virus (MuLV) and the subsequent expression of xenotropic as well as polytropic MuLVs. Generally, mice infected with any one of several groups of viruses, including MuLVs, have been shown to produce interferon (IF). However, we report here that AKR mice produce no IF, despite that fact that infectious, endogenous MuLV is expressed in these mice from birth.

AKR murine leukemia virus↗
PubMed1978

The genetic basis of susceptibility to leukemia induction in mice by 3-methylcholanthrene applied percutaneously.

Susceptibility to leukemia induction in mice by skin painting with 3-methylcholanthrene (MCA) is strain-specific, occurring only in strains relatively resistant to MCA-induced skin tumors. The Ah locus, which has a dominant allele (Ahb) for inducibility of the aryl hydrocarbon hydroxylase (AHH) enzyme system and a recessive allele (Ahd) for noninducibility, appears to be the major determinant of this trait. MCA-painted mice of strains and crosses carrying the Ahb allele usually show a high incidence of skin tumors (papillomas which may evolve into malignant tumors) and little or no leukemia, whereas in mice homozygous for the Ahd allele the treatment usually induces a high incidence of leukemia and few or no skin tumors. Among mice of a segregating backcross generation including both Ahb/Ahd heterozygotes and Ahd homozygotes, the occurrence of skin tumors was correlated directly with AHH inducibility and inversely with the leukemic response. Mice of Ahb strains with a high level of endogenous murine leukemia (MuLV) expression (C58, PL) show a much weaker skin tumor response than expected but no increase in leukemia incidence, and this observation tends to confirm the previous finding that MuLV infection of mice of low-MuLV strains results in reduced susceptibility to MCA tumorigenesis.

Animals↗
PubMed1977

Construction of a DBA/2.Fv-2r congenic strain. Apparent lethality of the homozygous Fv-2r genotype: brief communication.

From the (C57BL/6 X DBA/2)F1 cross, 13 serial backcrosses to the DBA/2 parental mouse strain were bred with selection by progeny testing in each generation for the Fv-2s/Fv-2r heterozygous genotype. Intercrossing heterozygotes of the 13th backcross generation produced no Fv-2r/Fv-2r homozygotes. Homozygosity for the Fv-2r allele thus appeared to be lethal on a DBA/2 background and in the absence of protector gene(s) of the C57BL strain.

Animals↗
PubMed1977

Mechanisms of the H-2 effect on viral leukemogenesis.

Evidence has been gathered which supports the notion that two distinct but interacting mechanisms, controlled by loci mapping within the H-2 complex, influence Friend murine leukemia virus (FV) disease. One mechanism, controlled by a gene mapping in or close to H-2D, influences the capacity of the H-2D gene product to form molecular complexes with FV molecules in the plasma membrane of infected cells. Formation of a complex appears to provide a target antigen for syngeneic cytotoxic T-lymphocytes, to cause co-capping of FV and H-2D antigens, to permit the selective inclusion of H-2Db molecules into progeny Friend virions, to influence the long-term maintenance of virus production in vitro and, in conjunction with the second mechanism, to stimulate the generation of cytotoxic T-lymphocytes. This second mechanism is controlled by a gene in the H-2K or H-2I region, and, in the presence of an H-2/FV molecular complex immunogen, influences the generation of H-2 restricted cytotxic T-lymphocytes and the rate of rejection of syngeneic FV-induced tumor cells.

Animals↗