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J D Feldman

Publications and source records attributed to J D Feldman.

At least 55 records · Page 3Linked to original sources
PubMed1978

Tumor-associated antigens of rat moloney sarcoma cells. II. Cytosol antigens.

Rat Moloney sarcoma cells (MST) were pulsed with 35S-L-methionine for 10 and 60 min and lysed by vortexing in 0.5% deoxycholate, 0.5% NP40, 0.02 M Tris, 0.05 M NaCl, pH 7.5, for 30 sec. The lysate was centrifuged at 16,300 X G for 10 min and the supernatant was co-precipitated with Ig fractions of normal BN serum, normal Lewis serum, BN antiserum to Moloney sarcoma cells (BNaMST), BN antiserum to tumor-associated antigens (BNaTAA), BN antiserum to murine leukemia virus (BNaMuLV), BN antiserum to p30 (BNap30), BN antiserum to gp70 (BNagp70), Lewis antiserum to BN (LeaBN), and BN antiserum to BC5 tumor (BNaBC5). With BNaTAA and BNaMST, a cytoplasmic TAA with m.w. 85,000 was detected. In addition, BNaTAA detected three other species of cytoplasmic TAA with m.w. 220,000, 170,000 and 39,000.

Animals↗
PubMed1978

Retino-tectal projections from half-ventral and half-dorsal eye rudiments in Xenopus.

When the ventral half of a developing eye in Xenopus larvae was removed at stage 32, the remaining fragment rounded up and developed into an eye which looked macroscopically normal by mid-larval stages. Eyes from half-dorsal rudiments were usually small, had more than one ventral fissure, and showed abnormal pupils. The contralateral retinotectal projection was always found to be normally ordered when mapped in later tadpole stages, or, just after metamorphosis. No mirror-image duplicated maps were seen, as was found previously in eyes deriving from half-nasal and half-temporal rudiments. It is concluded that the 'rule of distal transformation' does not apply to eyes which are generated from embryonic rudiments.

Animals↗
PubMed1978

p30-Anti-p30 immune complexes: intravascular clearance and extravascular sequestration in rats bearing Moloney sarcoma.

Complexes of 125I p30, a viral core polypeptide, and rat anti-p30 antibody, preformed in vitro, were injected into the heart of BN rats bearing Moloney sarcomas (MST) and of BN rats bearing an unrelated tumor or unexposed to tumor. Complexes were cleared from the circulation of MST-bearing rats more rapidly than from sera of controls and were almost completely eliminated after 30 hr. There was no relationship between rate of disappearance and size of tumor or levels of circulating complexes. Disappearance rates in rats with progressing and regressing tumors were similar. Uncomplexed labeled p30 was cleared from the circulation of tumor-bearing and control rats with kinetics similar to those of labeled complexes. Complexes were localized in the spleen of tumor-bearing and control rats, but much more in spleens of MST-bearing rats. No other tissues, including tumor, concentrated complexes, nor was there binding to peripheral blood and spleen cells. The data suggest that augmented clearance and sequestration were due to the formation of large insoluble complexes that were rapidly removed by the reticulo-endothelial system.

Animals↗
PubMed1978

Tumor-associated antigens of rat moloney sarcoma cells. I. Cell-surface antigens.

The dissociated cell surface membranes of a rat Moloney sarcoma (MST), derived from a BN rat, were extracted with 2 M KI, with 6 M guanidine thiocyanate, or by papain digestion. Extracts obtained with these three reagents were fractionated on columns of controlled-pore glass, 170 A pore size. A fraction was eluted from each preparation that contained tumor-associated antigens (TAA), viral, fetal, and histocompatibility antigens. With an antibody specific for TAA, the TAA, devoid of detectable viral, fetal, and histocompatibility antigens, were co-precipitated by addition of goat antibody to rat immunoglobulin. After electrophoresis, on slab gels, three bands were detected with estimated m.w. of 185,000, 150,000, and 70,000. No such bands were detected on slab gel electrophoresis with extracts of BC5, a chemically induced tumor, of normal BN lymphoid cells, of M-MuLV, or of fetuses, after incubation with anti-TAA antibody and goat antibody to rat immunoglobulin. TAA extracts prepared with 2 M KI, 6 M guanidine thiocyanate, or papain digestion showed immunologic reactivity. Cold TAA inhibited the co-precipitation of labeled TAA by rat antibody specific for TAA; they elicited antibody in guinea pigs but not in rats; and antibodies specific for TAA were cytotoxic to MST in the presence of C.

Animals↗
PubMed1977

Genetic association of the humoral and cellular immune responses of rats to Moloney sarcomas.

Brown Norway (BN), Lewis (Le), F1 hybrids of LexBN (LBN) and parent-to-LBN backcross rats were tested for cellular and humoral responses to a BN Moloney sarcoma. Regardless of AgB phenotype, BN backcrosses produced low levels of cell-mediated cytotoxicity (CMC) that were comparable to those of BN parents. Le backcrosses developed high levels of CMC similar to those produced in Le parents. An inverse relationship between levels of CMC and serum antibodies (cytotoxic for tumor cells and anti-p30 of MuLV) was observed; BN parents and backcrosses produced high levels of serum antibodies whereas levels in Le parents and backcrosses were low. LBN hybrids developed relatively high levels of CMC and serum antibodies. An additional finding was that the CMC response in Le parents and back-crosses was directed primarily against tumor-associated antigens rather than histocompatability antigens expressed on the tumor cells. The results suggest that humoral and cellular responses to Moloney sarcoma in rats are not determined solely by the major AgB histocompatibility locus but do have a genetic association. This genetic association was detected with a 51Cr release assay which detects T-cells, suggesting that select populations of effector T-cells may be genetically regulated.

Animals↗
PubMed1977

Sequential quantitation of circulating immune complexes in syngeneic and allogeneic rats bearing Moloney sarcomas.

A Raji cell radioimmunoassay was employed to quantitate serially circulating immune complexes (CIC) in the sera of syngeneic BN rats and allogeneic Lewis rats bearing BN Moloney sarcomas. In syngeneic BN hosts the levels of CIC attained and the time-course of detection were related to the tumor dose, tumor mass, and regressive or progressive course of the tumor. In general, syngeneic rats that received larger tumor doses developed larger tumors and greater maximum levels of CIC. However, the amount of CIC was not always directly proportional to the tumor size, although this was nearly the case with regressor BN and Lewis rats. In rats with regressing tumors, CIC decreased to insignificant levels as the tumors disappeared. Progressor BN rats that received 20 and 10 X 10(6) tumor cells had higher and more sustained levels of CIC, but, shortly before the hosts died, despite an increase of tumor size, there was a decline of CIC. Progressor BN rats that received an initial inoculum of 0.5 X 10(6) tumor cells that grew to 44 mm maximum mean diameter had levels of CIC which were only slightly above levels of control rats. All allogeneic Lewis hosts rejected BN Moloney sarcomas, but had transient low levels of CIC coincident with tumor growth. Lewis rats had lower levels of CIC than BN rats bearing comparable masses of sarcoma.

Animals↗
PubMed1977

Effect of macrophages and antibodies on in vivo growth of Moloney sarcoma in the rat.

Brown Norway and Lewis rats were challenged with a Brown Norway Moloney sarcoma tumor, MST-1, admixed with nonimmune peritoneal exudate macrophages syngeneic to the host; or admixed with nonimmune peritoneal exudate macrophages and hyperimmune anti-MST-1 antibodies. In vivo growth of MST-1 in BN and Lewis rats was inhibited by admixing Brown Norway or Lewis macrophages, respectively, with BN anti-MST-1 antibodies. The inhibiting BN antibodies were of the IgG2 class, lacking IgG2a antibodies. Brown Norway anti-MST-1 of IgG2 class without macrophages did not affect growth of MST-1. Brown Norway and Lewis anti-MST-1 antibodies of IgG2a class enhanced tumor growth, whether admixed with macrophages or not. Anti-MST-1 antibodies of IgM and IgG1 classes did not influence tumor growth. Peritoneal exudate macrophages removed from Lewis donors 8 to 10 days after inoculation of MST-1 inhibited completely growth of the challenge tumor; macrophages of Brown Norway origin were inhibitory only when harvested from hyperimmune donors, that is, 40 or more days after inoculation of MST-1. Macrophages from hyperimmune donors were specifically cytotoxic to MST-1 and did not inhibit an unrelated syngeneic BN tumor of chemical origin.

Animals↗
PubMed1976

Genetic role of rat macrophage cytotoxicity against tumor.

Macrophages from the Lewis (Le) rat strain are significantly more cytotoxic to a Moloney sarcoma tumor both in vivo and in vitro, than are macrophages from the Brown Norway (BN) strain. Activity of macrophages from (Le x BN)F1 rats that are histocompatible with the Moloney sarcoma tumor is directed toward tumor and/or virus-associated antigens and is expressed as a dominant genetic trait. Experiments with backcross rats suggest that the genetic factors are unrelated to the major histocompatibility locus (AgB) of the rats. BN microphages, although not active against tumor and/or viral antigens, can become cytotoxic to cells displaying Le alloantigens.

Animals↗
PubMed1976

Immunopathology.

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Allergy and Immunology↗
PubMed1976

Altered lymphocyte functions in rats bearing syngeneic Moloney sarcoma tumors. I. Mitogen responses, mixed lymphocyte reactions (MLR) and mixed lymphocyte-tumor reactions (MLTR).

Impairment of mitogen responses to Con A and LPS and of MLR and MLTR was detected in the spleens of rats bearing syngeneic Moloney sarcoma tumors. Depressed responses of both T cell and Ig+ cell populations were observed. During the observation period of 6 to 10 days post-tumor inoculation when maximal T cell-mediated cytotoxicity was observed in spleen and draining lymph node cells, spleen cells showed marked impairment in response to stimuli mentioned above. By contrast, draining lymph node cell activity was either unaltered or somewhat elevated above the level of activity measured in normal control populations. Data presented in this and an accompanying paper strongly indicate that macrophages are activated as immunosuppressor cells in tumor-bearing rats.

Animals↗
PubMed1976

Distribution of viral glycoprotein gp 69/71 on cell surfaces of producer and nonproducer cells.

The distribution of the viral glycoprotein, gp 69/71, was studied on the cell surfaces of virus-producing and nonproducing cells. gp 69/71 was distributed evenly on cell membranes and on viral membranes of cells producing murine leukemia virus. gp 69/71 was distributed uniformly on cell membranes of thymocytes from NZB and strain 129 mice but was not detected on cell membranes of BALB/c thymocytes. Viral particles were associated with NZB and BALB/c thymocytes but were not in or on 129 thymocytes. We conclude that the presence of gp 69/71 on thymocyte membranes is not related to virus production. In the strains showing gp 69/71 on their thymocyte surfaces (NZB and 129), a large percentage of the thymocytes are positively labeled, all more or less equally. Immunochemical analysis of cell surface proteins labeled with 125I corroborated the ultrastructural observations. Thus, gp 69/71 can be expressed on the surface of thymocytes independently of virus particle production.

Animals↗
PubMed1976

Altered lymphocyte functions in rats bearing syngeneic Moloney sarcoma tumors. II. Suppressor cells.

Spleens from tumor-bearing rats contained a population of adherent cells that suppressed lymphocyte responses to Con A and LPS and cell-mediated cytotoxicity (CMC). By use of various fractionation procedures, Ig+ cells, T cells, and null cells were excluded as candidates for the suppressor cell activity. Procedures that removed macrophages abolished the suppressive activity whereas those procedures that enriched for or involved direct addition of macrophages resulted in augmented suppression. On the basis of these results, we conclude that the suppressor elements in spleens of tumor-bearing rats were macrophages.

Animals↗
PubMed1975

Cell-mediated cytotoxicity to moloney sarcoma in syngeneic and allogeneic rats.

Cell-mediated cytotoxicity in the primary immune response to Moloney sarcoma tumor (MST) in allogeneic and syngeneic rats was found to be predominantly T-cell-dependent. A minor non-T-cell cytotoxic activity may also have been detected. CMC was presumably directed against tumor and viral related antigens in the syngeneic host and primarily against alloantigens in the allogeneic host. CMC was more virgorous in the syngeneic host. This may be due to differences in quantities or immunogenicities of the various antigens involved. Two peaks of T-cells in effector populations were observed during a 20-day post-inoculation period. The first peak corresponded to peak T-cell-mediated cytotoxicity on day 8 and the second peak occurred on days 13 or 14 when CMC was minimal or undetectable.

Animals↗
PubMed1975

Alloantigen expression of a rat Moloney sarcoma.

Cells of a brown Norway (BN) rat Moloney sarcoma (MST) failed to express certain BN alloantigen specificities and bound only about 30-50% the amount of labeled alloantibody bound by normal BN spleen cells. MST cells lacked antigen specificities shared by BN and WF rats, but expressed some of the antigen shared by BN and AUG rats. Further loss of alloantigens that occurred with prolonged in vitro culture was associated with reduced virulence of MST cells for syngeneic hosts and with increased expression of tumor-associated antigens. The LEW rats, which are resistant to MST cells, might have rejected the tumor on the basis of factors other than Ag-B antigens.

Animals↗