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Biomedical subjects

M Tuffrey

Publications and source records attributed to M Tuffrey.

At least 37 records · Page 2Linked to original sources
PubMed1984

Reinfection of the mouse genital tract with Chlamydia trachomatis: the relationship of antibody to immunity.

Progesterone-treated CBA mice which had had genital infections with a fast, human strain of Chlamydia trachomatis either 8, 16, 58, or 69 weeks previously were rechallenged through the uterine wall, along with groups of untreated controls. Serum IgG antibody and/or local IgA antibody was measured using a micro-immunofluorescence technique. Although the infection was self-limiting, chlamydiae were cleared significantly more quickly from the previously infected groups than from their controls in all experiments. However, mice which had had a previous infection recently and which had high titres (geometric mean 1: greater than or equal to 2048) of serum IgG antibody and local IgA antibody immediately before rechallenge, were as susceptible as mice which had had a distant past infection and which had much lower titres (geometric mean 1:48) of serum IgG antibody. Thus, some immunity was induced in the mouse model, but pre-existing antibody seemed to be of little importance in this, and did not influence the initial susceptibility to reinfection.

Animals↗
PubMed1982

Genital-tract infection and disease in nude and immunologically competent mice after inoculation of a human strain of Chlamydia trachomatis.

A fast, human strain of Chlamydia trachomatis was introduced into the uterus of progesterone-treated CBA mice and congenic CBA nude mice through the uterine wall or via the cervical canal. The numbers of inclusions produced by samples taken from the vagina of the nude mice were significantly greater (P less than 0.05) than those produced by samples from immunologically competent normal mice. However, the infection was self-limited, lasting about 60 days, and there was no statistical difference in its duration in the nude and normal mice despite the failure of the former to mount a chlamydial antibody response. In contrast, 14 of 18 normal mice had developed a 4-fold or greater rise in the titre of IgG antibody 14 days after inoculation. A serum titre of 1:512 or greater was attained in 15 of these mice, and high titres persisted for 69 days or longer after inoculation. The numbers of polymorphonuclear leucocytes in vaginal smears from both normal and nude mice increased by 12 days after inoculation, indicating an inflammatory cell response. However, interpretation of the cellular response after the 40th day was difficult because of recommencement of the oestrous cycle. The results indicate that T lymphocytes and T-lymphocyte-dependent antibody have little effect on the course of the self-limited chlamydial genital infection.

Animals↗
PubMed1981

Absence of activated murine leukaemia virus in x-irradiated CBA/H-T6crc mice.

CBA/H-T6Crc mice, a substrain that does not normally express demonstrable levels of murine leukaemia virus (MuLV) and has a low natural incidence of leukaemia, were examined for evidence of virus activation at various times following X-irradiation. Although X-irradiation caused a high incidence of leukaemia, no ecotropic, xenotropic or recombinant MuLV was detected by in vitro co-cultivation of bone marrow, spleen and thymus cells from pre-leukaemic and leukaemic animals with selectively permissive cell lines followed by indirect immunofluorescence for MuLV group-specific (gs) antigen. These results, therefore, are not consistent with the hypothesis that endogenous viruses are the universal aetiological agents of leukaemia.

Animals↗
PubMed1980

The use of 125I-labelled protein A for the detection of humoral immunity to gross murine leukaemia virus.

A solid-phase radioimmunoassay utilising bind of 125I-labelled protein A to antibodies bound to virus adsorbed onto microtitre plates was shown to be suitable for detection of humoral immunity to Gross murine leukaemia virus (MuLV). The specificity of the reaction was shown by the fact that only homologous or closely related viruses effectively inhibited binding of antibodies to adsorbed virus. With this method a low level of spontaneous humoral immunity was demonstrated in sera from AKR/Crc mice, a strain with high concentrations of endogenous virus, whereas little or no anti-viral activity was found inCBA/H-T6Crc, a subline that does not appear to express MuLV.

AKR murine leukemia virus↗
PubMed1979

Absence of ecotropic or recombinant murine leukaemia virus in preleukaemic and leukaemic X-irradiated NZB mice.

NZB mice X-irradiated with a single dose of 630 R when they were 1-month old developed a high incidence of histologically defined lymphocytic leukaemia 8--25 weeks later. We have screened for murine leukaemia viruses (MuLV) in the lymphoid tissues of 8 of these leukaemic mice, and in 8 "preleukaemic", apparently healthy NZBs killed 1 month post irradiation. Xenotropic, but not ecotropic or recombinant MuLV, was detected by in vitro co-cultivation of bone marrow, spleen and thymus with selectively permissive cell lines, followed by the immunofluorescence test for MuLV gs antigen, and the XC test. Our results are not consistent, therefore, with the concept that the factor causing the leukaemias was an oncogenic virus activated by X-irradiation.

Animals↗
PubMed1976

Murine leukaemia virus group-specific antigen in tumor-resistant tetraparental AKR reversible CBA/H-T6 chimaeras.

Various facts are now known about the relative lymphoma resistance of a group of tetraparental AKR reversible CBA/H-T6 chimaeras derived by early embryo aggregation. Firstly, their tumour resistance is not due to the lack of the lymphomaprone AKR cells. Secondly, results showing titres of MuLV-gs antigen comparable with, and occasionally in excess of, those in the AKR suggest that the tumour resistance of the chimaeras is unlikely to be due to a lack of oncogenic leukaemia virus. However, in marked contrast to the AKR, antibody-viral antigen renal complexes in the chimaeras were minimal. Lack of viral antigens could not explain the relative lack of renal complexes. Absence of the corresponding anti-viral antibody is the most likely explanation and this has to be attributed to the CBA component of the tetraparental AKR reversible CBA/H-T6 chimaeras. We suggest that with tolerance to the leukaemia virus being maintained and in the absence of anti-viral antigenic complexes, tumour-specific sites can be recognized and thus tumours are eliminated. This hypothesis remains to be proven.

AKR murine leukemia virus↗
PubMed1976

The innate resistance of CBA mice to endogenous murine leukaemia virus infection.

The incidence of lymphomata in CBA mice is low and furthermore is unaltered by transplantation at the early blastocyst stage and being born from the lymphoma-prone AKR. The number of C-type murine leukaemia virus particles in CBA derived in this manner and milk-fostered by AKR mice in no way differs from normal CBA. The results suggest that the oncogenic Gross virus does not pass through either the transplacental or transmammary routes, or alternatively that viral replication in the CBA was in some way inhibited. Both possibilities have still to be distinguished.

Animals↗
PubMed1976

Failure to suppress theta antigenic expression in progeny derived from pre-immunized maternal recipients.

One possible theory concerning the success of the fetus as an allograft has been attributed to maternal modification of foreign fetal antigenic expression. In this respect progeny derived from pre-immunized maternal mouse recipients, have been examined for any modification (reduction) of corresponding theta antigen determinants. Two major groups of mice were examined. The first group of embryo transplantation derived AKR homozygotes born from pre-immunized CBA recipients whilst producing the corresponding anti-thetaAKR antibody activity. The second group of naturally derived reciprocal (CBA x AKR)F1 heterozygotes were also born from pre-immunized maternal recipients. In neither group was theta expression found to be modified and the significance of this finding is discussed in respect of other situations where fetal antigenic expression is known to be altered by maternal influence.

Animals↗
PubMed1976

Transmission of auto-immune haemolytic anaemia and murine leukaemia virus in F1 (BALB/c X NZB) hybrid mice derived by ovum transplantation.

F1(BALB/c X NZB)hybrid progeny derived by ovum transplantation were used to study the transmission of auto-immune haemolytic anaemia and murine leukaemia virus (MuLV) by male New Zealand black (NZB) mice. Fertilized ova, collected from the normal BALB/c partners 3 1/2 days after mating, were transferred to other, surrogate, BALB/c mothers, which then carried, delivered, and reared the hybrid young. This technical manoeuvre effectively closed the congenital transplacental route theoretically available to any infectious MuLV originating from the NZB father. Nevertheless, such progeny developed exactly the same profile of auto-immune haemolytic disease and the same range of diverse malignancies as their normally-derived F1(BALB/c X NZB) counterparts, and they carried type C MuLV particles readily detectable by electronmicroscopy. We concluded, therefore, that both the auto-immunity and virus were transmitted before placentation, presumably by the NZB male at fertilization, and probably as genetic information.

Anemia, Hemolytic, Autoimmune↗
PubMed1975

Failure to detect antibody against Gross virus in tetraparental AKR reversible CBA mouse chimaeras.

In spite of early acquisition upon the germ line, tolerance to the Gross (gs) virus is short-lived in the AKR. From about the age of 3 months anti-gs antibodies occur and these complex with the corresponding viral antigens. Such complexes are best seen in the glomeruli by means of immunofluorescence. In marked contrast to the AKR, renal complexes were minimal in a group of AKR reversible CBA/H-T6 chimaeras derived by early embryo aggregation. This was particularly surprising since large numbers of type C murine leukaemia virus-like particles were identified in the chimaeras and the tissues were found to be saturated with gs antigen. The lack of renal antigen-antibody complexes was the first suggestion that anti-gs antibody might not be present in the chimaeras and renal elution studies here support this assumption. In contrast to the AKR where "split " renal eluates have been shown to have anti-gs activity, no activity was demonstrated in eluates from any of the chimaras. Tolerance to the oncogenic Gross virus in the chimaeras has to be attributed to the CBA parental strain component and since this component is also held responsible for the tumour resistance of these chimaeras, both phenomena could well be related. In this context it would appear that in the absence of masking by antibody viral antigenic complexes, tumour specific sites can be recognized in the chimaeras and unlike the AKR "normal" tumour immunity can be effected. This hypothesis is currently bei-ng tested.

AKR murine leukemia virus↗