Biomedical subjects
Publications and source records attributed to F F Richards.
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Plasmacytomas are induced in BALB/c mice by the intraperitoneal injection of pristane (2,6,10,14-tetra-methylpentadecane) after a latent period of six months and more [Anderson, P. N. & Potter, M. (1969) Nature 222, 994-995]. Spleen cells mesenteric lymph node cells, thoracic lymph node cells, and peritoneal exudate cells were prepared from pristane-treated and control uninjected BALB/c mice during the course of a 10-month period, and these cell suspensions were tested for the release of infectious murine leukemia viruses. Endogenous ecotropic and xenotropic murine leukemia viruses were expressed in pristane-treated mice during the latter part of the tumor induction period, in those cell populations in which transformed plasma cells appear, namely, peritoneal exudate cells and thoracic lymph node cells. The significance of preferential expression of both ecotropic and xenotropic murine leukemia virus in target cell populations following the administration of a carcinogen is discussed in terms of the possible formation of an oncogenic variant virus.
Mice of the low leukemia (BALB/cJ x A/J)F1 hybrid (CAF1) strain express B-and N-tropic infectious murine leukemia virus (MuLV) after the age of 6 mo. Initation of a protracted immunological disorder, the graft-versus-host reaction (GVHR), at 7 wk of age, accelerates the induction of both these mouse-tropic endogenous viruses, and preferentially enhances the replication of B-tropic MuLV. The earlier appearance of B-tropic MuLV in a greater proportion of mice and in higher titer is thought to be casually related to the eventual development of lymphoreticular tumors in the GVHR mice, since previous studies have shown that these same tumors can be reproduced by inoculating syngeneic recipients with serially passaged GVHR extracts containing B-tropic MuLV.
The L-asparagine analogue 5-diazo-4-oxo-L-[5-14C]norvaline binds irreversibly to the active site of Escherichia coli L-asparaginase. Conditions for optimal labeling in buffers containing 50% dimethylsulfoxide have been developed and kinetic parameters of the inactivation have been determined. After reduction, alkylation and subsequent degradation of the modified enzyme with alpha-chymotrypsin, the principal radioactive decapeptide of sequence Val-Gly-Ala-Met-Arg-Pro-Ser-Thr-Ser-Met was isolated. A second radioactive hexapeptide Arg-Pro-Ser-Thr-Ser-Met resulting from chymotryptic digestion of the decapeptide was also isolated. Evidence is presented for the attachment of the 5-diazo-4-oxo-L-norvaline residue to serine-9 in the decapeptide via an acid-labile linkage.
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When mice are sequentially immunized with two antigens to give an oligoclonal "double-binding" antibody response, there is a concomitant increase of "double-binding" cell surface receptors on their splenic lymphocytes. Competition studies suggest that the capacity to bind the two ligands, bovine pancreatic ribonuclease (EC 3.1.4.22) and a 2,4-dinitrophenyl (DNP) derivative, is a function of the same molecules. In ribo-nuclease-primed mice, an early response to bovine gamma globulin containing an average of 60 Dnp groups per molecule is the appearance of an increasing number of cells bearing surface receptors binding both ribonuclease and Dnp. Later, these double-binding cells are diluted by cells that bind Dnp, but not ribonuclease. The analogous phenomenon is observed when the two antigens are used in reverse order. While other reports suggest that there may be several different receptors in relatively undifferentiated cells from unimmunized mice, it seems likely that cells committed to antibody production carry a predominant multispecific cell surface immunoglobulin receptor.
Cellfree extracts (CFEs) prepared from (BALB/cJ X A/J)F1 (CAF1) and (BALB/cJ X C57BL/6J)F1 (CB6F1) mice in which a graft-versus-host reaction (GVHR) has been induced are known to be oncogenic, but only after a protracted latent period (mean, 16 mo). Serial passage of such CFEs in successive generations of syngeneic mice inoculated at birth led to the development of two separate oncogenic preparations, the CA serioes in CAF, mice and the CB series in CB6F, mice, in which the mean latent period was reduced to 6 and 12 months, respectively. Both oncogenic preparations contained infectious B-tropic murine leukemia virus (MuLV) and particles with the ultrastructural characteristics of MuLV. No other kind of virus particle was seen. When these preparations were injected into infant syngeneic mice, B-tropic MuLV could be detected in the reticular tissues as early as 2 weeks thereafter. The virus persisted in the reticular tissues and was present in the lymphoreticular tumors that subsequently developed. However, if the same preparation was injected into young adult recipients, there may have been transient MuLV replication, but the virus subsequently disappeared from the reticular tissues and no lymphoreticular tumors developed. Previous experiments showed that MuLV was present in CFEs prepared from CAF, animals with the GVHR but absent in those of normal control mice. Since the lymphoreticular tumors arising in mice with the GVHR were the same as those induced by the CA and CB MuLV preparations, it was concluded that tumorigenesis in mice with the GVHR was caused by endogenous B-tropic MuLV activated by the immunologic disturbance.
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Murine lymphoid cells were infected in vitro with WN 1802 B, a naturally occurring murine leukemia virus isolated from the spleen of an 18-month-old BALB/c mouse. Normal spleen and bone marrow cells were more susceptible to infection than were cells prepared from thymus and lymph node. Spleen cells from athymic nu/nu mice also could be readily infected with virus. Permissive cells did not ingest iron readily infected with virus. Permissive cells did not ingest iron filings and did not adhere to plastic. Exogenous replication of murine leukemia virus was enhanced in spleen and lymph node cells treated with lipopolysaccharide, a bone marrow-derived lymphocyte mitogen. Conversely, cells treated with the thymus-derived lymphocyte cell mitogens, phytohemagglutinin and concanavalin A, were less capable of supporting murine leukemia virus replication. These studies suggest that the natural host for WN 1802 B is the bone marrow-derived lymphocyte.
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IgG New binds ligands such as orceine, menadione, and uridine with a low affinity (K(0) about 1 x 10(3) liter/mol) and a gamma-hydroxy derivative of vitamin K(1) with a higher affinity (K(0) = 1.7 x 10(5) liter/mol). Binding studies indicate that both the 2-methylnaphthoquinone rings and the phytyl tail of the vitamin K(1) hapten contribute to the total binding energy. The binding of these ligands in the crystalline state has been investigated by difference Fourier maps of Fab' New-ligand complexes at 6-A resolution. A 3.5-A resolution difference Fourier map obtained for the gamma-hydroxy derivative of the vitamin K(1)-Fab' complex shows that this hapten is bound in a shallow groove or crevice between the light and the heavy chains, in close proximity to the polypeptide segments containing the hypervariable regions. At least 12 amino-acid residues from both the light and the heavy chains appear to be in close contact with the ligand. No major conformational changes were detected in the Fab' fragment after ligand binding.
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