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F Lilly

Publications and source records attributed to F Lilly.

At least 91 records · Page 5Linked to original sources
PubMed1974

Cell surface antigen induced by Friend murine leukemia virus is also in the virion.

Intact particles of Friend leukemia virus derived from infectious mouse serum absorb only trace amounts of cytotoxic anti-FMR antibodies, but physical disruption of the virions by freezing and thawing, by ether extraction or by detergent treatment releases large amounts of FMR antigenic activity. Thus this antigen, previously considered to occur mainly as a neo-antigen on the surfaces of virus-infected cells and as a soluble substance in the serum of infected mice, may be primarily a virion component.

Animals↗
PubMed1973

Relation of chromosome 4 (linkage group 8) to murine leukemia virus-associated antigens of AKR mice.

Genes specifying or controlling the expression of G(IX) (cell surface), GCSA (cell surface), and gs (internal viral) antigens are located in chromosome 4 (linkage group [LG] VIII) of the AKR mouse. All three antigens may exhibit mendelian inheritance, mice being antigen positive or antigen negative, but each may also appear in leukemic cells of mice whose inherited genotype was antigen negative. The G(IX)-determining gene in LG VIII of AKR mice apparently is equivalent to Gv-1, which determines expression of the same antigen in 129 strain mice, but which in the latter strain is located in LG IX. As the estimated distance of Gv-1 from H-2 in 129 mice is considerable (37 units) further tests are now indicated to assess the possibility of pseudolinkage in this case. The Fv-1 locus, also located in LG VIII, influences the mouse's titer of MuLV, and might thereby be thought to regulate the G(IX) and gs phenotypes of AKR backcross segregants. But the data indicate a discrete LG VIII locus for G(IX), since expression of this antigen is mendelian and independent of infectious virus titer. Since the G(IX) and GCSA phenotypes of AKR backcross segregants were invariably concordant, these two antigens must be specified or controlled by closely linked genes, and the latter also is presumably independent of virus titer. The question as to what extent expression of gs antigen in the segregants is secondary to virus production is undecided.

Animals↗
PubMed1973

Independence of H-2K and H-2D antigenic determinants on the surface of mouse lymphocytes.

At 37 degrees C, fluorescein-conjugated anti-H-2 alloantibodies specifically induce, at the surface of living mouse lymphocytes, the redistribution of the corresponding H-2 antigens, which cluster as patches and sometimes single caps at one pole of the cell. This aggregation is inhibited at 0 degrees C and the H-2 antigens, stained by fluorescent antibodies in the cold, appear evenly spread over the cell surface. This phenomenon was used to define the relationships between the membrane structures bearing the antigens coded by the H-2K and the H-2D genes of the H-2 region. Monospecific anti-H-2 antibodies coupled to either tetramethyl rhodamine isothiocyanate or fluorescein isothiocyanate were used to induce the redistribution of H-2D and H-2K antigens of the H-2(b) and H-2(k) haplotype at the surface of lymph node cells from homozygous and F(1) hybrid mice. It was observed that the diffuse distribution of H-2K antigens labeled at 0 degrees C was not affected by the prior antibody-induced aggregation of H-2D antigens and vice versa. The results were the same for H-2 antigens governed by genes located either in cis or in trans position. These data indicate that the H-2K and H-2D antigens migrate independently at the cell surface, and suggest that the gene products from the D and the K end of the H-2 region are expressed on independent molecules or structures at the cell membrane.

Animals↗
PubMed1971

A major genetic locus affecting resistance to infection with murine leukemia viruses. II. Apparent identity to a major locus described for resistance to friend murine leukemia virus.

The N-B locus affecting tissue culture infectivity with naturally occurring murine leukemia viruses appears to be identical to the Fv-1 locus described for sensitivity to Friend leukemia virus. Results of tissue culture studies were parallel to results of studies in vivo and indicate that the F-S virus is N-tropic and the F-B virus is NB-tropic. Inbred and partially congenic mouse strains sensitive at Fv-1 show N-type sensitivity; strains resistant at Fv-1 show B-type sensitivity. The Fv-2 locus does not appear to exert significant effect in tissue culture. Knowledge of N-B type has been useful in predicting Fv-1 sensitivity.

Animals↗
PubMed1970

Acceleration by thymosin of the development of resistance to murine sarcoma virus-induced tumor in mice.

The development of resistance to progressive tumor growth and the effect of a thymic extract upon this developmental process were examined in CBA/Wh mice. Inoculating mice of various ages with murine sarcoma virus (Moloney) permitted the assessment of the period of time postnatally at which the animals developed a threshold level of resistance to progressive tumor growth. Resistance in CBA/Wh mice, at the virus dose used, was first detected at approximately two weeks of age and was completely developed at five weeks.Thymosin, a soluble calf thymic fraction, when administered to neonatal mice beginning on the second day of life, significantly accelerated the rate of development of resistance to progressive tumor growth. The data suggest a humoral role for the thymus in the development of tumor immunity, and that the normal development of cell-mediated immunological competence can be accelerated through the use of thymus-derived extracts.

Age Factors↗