Search PubMed⌕ Search

Biomedical subjects

T Aoki

Publications and source records attributed to T Aoki.

At least 1,243 records · Page 69Linked to original sources
PubMed1973

Leukemia-associated transplantation antigens related to murine leukemia virus. The X.1 system: immune response controlled by a locus linked to H-2.

Two BALB radiation leukemias are strongly rejected by hybrids of BALB with certain other mouse strains, although BALB mice themselves exhibit no detectable resistance whatever. Hybrids immunized with progressively increased inocula are resistant to 200 x 10(6) or more leukemia cells; their serum is cytotoxic for the leukemia cells in vitro and protects BALB mice against challenge with these BALB leukemias. The antigenic system thus identified has been named X.1. In (BALB x B6) hybrids the major determinant of resistance was shown to be a B6 gene in the K region of H-2. This is likely to be the Rgv-1 (Resistance to gross virus) locus of Lilly, which may thus be identified in this case as an Ir (Immune response) allele conferring ability to respond to X.1 antigen on MuLV and leukemia cells, and so responsible for production of X.1 antibody and the rejection of X.1(+) leukemia cells by hybrid mice. Immunoelectron microscopy with X.1 antiserum (from immunized hybrids) shows labeling both on the cell surface and on virions produced by the leukemia cells. It is not known whether X.1 comprises only one or more than one antigen. Three radiation-induced BALB leukemias, one A strain radiation-induced leukemia, and 15/15 AKR primary spontaneous leukemias were typed X.1(+) by the cytotoxicity test. Several other leukemias, including one induced by passage A Gross virus and one long-transplanted AKR ascites leukemia carried in (B6 x AKR)F(1) hybrids, were X.1(-). Normal mice of strains with a high incidence of leukemia and one other strain (129) express X.1 antigen, but evidently in amounts too small for certain detection in vitro; by the method of absorption in vivo, however, these strains could be typed X.1(+) and other strains X.1(-). We ascribe the X.1 antigen system tentatively to a sub-type of MuLV that is not passage A Gross virus and is probably not the dominant sub-type in strains with a high incidence of leukemia. After repeated passage in hybrids, one of the BALB leukemias became relatively resistant to rejection by the hybrid, partially lost its sensitivity to X.1 antiserum in vitro, and in electron micrographs was seen to produce fewer virions. The serum of untreated (BALB x B6) hybrids often contains cytotoxic antibody against leukemia cells, some of it probably anti-X.1. But another commonly occurring antibody, which is cytotoxic for C57BL leukemia EL4, appears to belong to another (undefined) system.

AKR murine leukemia virus↗
PubMed1973

Demonstration of a cell-surface antigen associated with murine sarcoma virus by immunoelectron microscopy.

Cells transformed by murine sarcoma virus have been examined for the presence of a new virus-associated cell-surface antigen by immunoelectron microscopy. A common antigen has been detected on the surface of nonproductively transformed cells that were induced by two different strains of murine sarcoma virus, Kirsten and Moloney. This antigen shows crossreaction with cell lines transformed by murine sarcoma virus that were produced in two different mammalian species, rats and mice. Further, this antigen is distinct from previously described antigens on the surfaces of cells infected by murine leukemia virus, on the viral envelope, and on the surfaces of spontaneously transformed cell lines or cell lines transformed by x-irradiation.

Animals↗
PubMed1973

Antigenic properties of endogenous type-C viruses from spontaneously transformed clones of BALB-3T3.

During long-term tissue culture of spontaneously transformed clones from BALB/c 3T3 mouse-embryo cells, some clones spontaneously begin to produce high titers of endogenous murine type-C viruses. The antigenic properties of these viruses have been analyzed by indirect immunoelectronmicroscopy and can be classified into two distinguishable populations: (a) BALB/c murine myeloma-associated extracellular viruses that carry a specific envelope antigen, xVEA, different from the typical murine leukemia viral envelope antigens; and (b) previously uncharacterized type-C viruses that have neither xVEA nor the murine leukemia viral envelope antigens. The former produces PC1 antigen and the latter might induce a new cell-surface antigen. Neither of these two populations of BALB/3T3 endogenous type-C viruses was able to infect BALB/c cells but both could infect NIH Swiss cells. A single BALB/3T3 clone, then, can release infectious endogenous type-C viruses with at least two different antigenic properties. We conclude that BALB/c somatic cells contain preexisting genetic information for production of at least closely related but, nevertheless, distinct type-C viruses.

Animals↗