Search PubMed⌕ Search

Biomedical subjects

J Fachet

Publications and source records attributed to J Fachet.

At least 55 records · Page 3Linked to original sources
PubMed1981

Stimulatory and inhibitory soluble mediators produced by stimulated lymphocytes and tested in human and murine in vitro systems.

The cellular origin and target specificity of two types of soluble mediators viz., the inhibitor of DNA synthesis (IDS) and the stimulator of DNA synthesis (SDS) have been studied. These mediators were produced by human and murine lymphocytes derived from different organs and stimulated by different mitogens, viz. phytohaemagglutinin (PHA-P), concanavalin A (Con A) and lipopolysaccharide (LPS). Their target effect was quantitated by assessing the 3H-thymidine incorporation of murine and human lymphocytes stimulated by different T and B cell mitogens (Con A, PHA and LPS). IDS activity was detected in supernatants of PHA stimulated lymphocytes originated from immunologically hyporeactive patients (tumor-bearing patients, pregnant women) in contrast to majority of control patients. Marked "SDS" activity was produced by normal lymphocytes as tested in human and murine lymphocytes stimulated by Con A or PHA, while IDS activity was detected if the target cells were stimulated by LPS. The effects of "SDS" failed to show species specificity using human and murine test-systems.

Adult↗
PubMed1980

Effect of lentinan on the production of migration inhibitory factor induced by syngeneic tumor in mice.

Attempts were made to reveal the mechanism of the inhibitory effect of lentinan on methylcholanthrene-induced transplantable fibrosarcoma (A/Ph.MC.SI) isografts. Since the involvement of a delayed-type hypersensitivity response can be supposed to operate against this syngeneic tumor, the enlargement of regional lymph nodes, the DNA synthesis activity and the migration inhibitory factor producing capacity of the regional lymph-node cells were studied in the control and lentinan-treated, tumor-bearing mice at different times after tumor implantation. The only parameter affected until the first sign of tumor inhibition on the 8th day was the MIF-producing capacity. Regional lymph-node cells in the lentinan-treated mice showed a peak response at this time while practically no MIF was produced by cells of non-treated mice. The early phase of the developing anti-tumor reaction (enlargement of and proliferation in the lymph nodes) was initiated in all recipients but only some of them could reject the tumor in the non-treated animals that rejected the tumors in all cases. It can be supposed that a tumor-induced immunosuppression emerges in the tumor-bearers and can be overcome by lentinan treatment, most likely through enhancement of the MIF production. For measurement of MIF activity a continuously dividing in vitro macrophage-like cell line was established and employed in the micro-wound migration assay.

Animals↗
PubMed1980

Effect of lentinan on tumor growth in murine allogeneic and syngeneic hosts.

The effect of lentinan on retardation and regression of transplanted tumors was analysed in allogeneic and syngeneic tumor-host systems. The effect of lentinan treatment was most variable in random-bred Swiss albino mice bearing sarcoma 180. With inbred host strains, it was most effective in A/PH and less, or not at all, in others (A.BY, A.CA, A.SW, DBA/2, BALB/c, C3H/Di, AKR, BIO, BIO.1, BIO.BR, BIO.D2). In order to eliminate the allogeneic differences, a syngeneic transplantable 3-methylcholanthrene-induced sarcoma (A/PhMC.SI) has been developed in the A/Ph strain, previously found to be the most responsive to lentinan. The growth of this sarcoma was dramatically inhibited and regression was detected in all lentinan-treated syngeneic recipients. Both the lentinan-treated and untreated regressor animals exhibited a high degree of resistance to a secondary challenge. However, the growth of a spontaneous, transplantable syngeneic adenocarcinoma in A/Ph mice was not influenced by lentinan treatment. The results presented substantiate further the conclusion that the effect of lentinan is mediated through host mechanisms, and show that these mechanisms are able to act against a syngeneic tumor.

Animals↗
PubMed1980

Gene affecting superoxide dismutase activity linked to the histocompatibility complex in H-2 congenic mice.

The activity of cyanide-sensitive, Cu-Zn superoxide dismutase (SOD) was studied in liver sytosols from H-2 congenic strains of mice. Higher SOD activity was found in livers of mice having H-2b/A.BY, B10, and C3H.SW/haplotypes than in those of H-2a, H-2k and H-2d haplotypes. Segregation studies supported these correlations. In H-2 recombinant strains of mice, the genes influencing the liver SOD activity occur, as ascertained by mapping techniques, at or near the H-2d region of the major histocompatibility complex.

Animals↗
PubMed1979

Differences in [3H]-thymidine uptake of lymph node cells stimulated by Con A and PHA in H-2 congenic mouse strains.

The genetic control of the lymphocyte responsiveness to Con A and PHA-P has been studied by using inbred, H-2 congenic mouse strains. Segregation studies were carried out on F1 and backcross mice of a high and a low responder strain. According to the results, there is a strong correlation between the responsiveness of lymph node cells to mitogens and H-2 haplotypes in different H-2 congenic strains of mice and in different backcross generations. High responsiveness to PHA-P is associated with H-2b, while low responsiveness with H-2a or H-2k haplotypes, but the correlation is the inverse in response to Con A, in the parental strains and backcross mice as well. The magnitude of the responses to both Con A and PHA-P was found to be intermediate in F1 heterozygotes of a low and high responder parental strain. The effect of other non H-2 genes on the responsiveness to these mitogens has also been demonstrated.

Animals↗
PubMed1978

Changes in mouse liver superoxide dismutase activity and lipid peroxidation during embryonic and postpartum development.

In inbred mice possessing 'high' and 'low' tissue superoxide dismutase (SOD) activity, it was observed that the difference in the SOD activities of the liver homogenates during development attains the maximum characteristic of the strain by about the 150th day. Subsequently, the SOD activity change displays a tendency in contrast with the age and the basic state. In the course of the development, a difference was also observed between the 2 mouse strains in the lipid peroxidation variation.

Animals↗
PubMed1978

Correlations between the genetic control of natural and oxazolone-induced antibody production.

Nonimmune sera of inbred and H-2 congenic mouse strains contain natural antibodies of the IgM type reacting with 4-(ethoxymethylene)-2-phenyloxazolin-5-one (oxazolone). The genetic regulation of the level of natural and induced antibodies to oxazolone was compared. High natural antibody-producing ability was inherited recessively, while high oxazolone-induced IgM antibody formation was dominant in F1 animals. Studies on nude mice demonstrated that T cells do not affect the natural antibody level, but were required for induced antibody production. Breeding studies and linkage analysis revealed multigenic control and a significant role of allotype-linked genes in both cases. Furthermore, the influence of H-2 linked genes on induced primary IgM antibody production was demonstrated.

Animals↗
PubMed1978

Sensitivity to glucocorticoids of lymph node cells stimulated in vivo by oxazolone.

Sensitization of B10.A mice with oxazolone results in delayed-type hypersensitivity (DTH) and a two to three-fold increase in the weight of regional lymph nodes by the third day. Hydrocortisone treatment of the animals 3 days after sensitization suppresses the manifestation of DTH on the tenth day but not on the seventieth day and significantly decreases the weight of lymph nodes both in control and oxazolone-sensitized mice. The regional lymph node cells of oxazolone-stimulated mice were, like the controls, sensitive to dexamethasone in vitro, as judged by viability and thymidine incorporation. Dexamethasone binding capacity of the regional lymph node cells 72 h after oxazolone sensitization increased. However, the dissociation constant for dexamethasone, the binding specificity, and the nuclear transfer of the hormone were not altered. Since high doses of hydrocortisone given 3 days after sensitization were unable to erase permanently the DTH to oxazolone, it seems very likely that cells responsible for the immunological memory survive the high dose of hydrocortisone.

Animals↗
PubMed1977

Genetic control of contact sensitivity to oxazolone in inbred, H-2 congenic and intra-H-2 recombinant strains of mice.

Delayed-type hypersensitivity (DTH) to 2-phenyl-4-ethoxymethylene-5-oxazolone (oxazolone) was found to be under multigenic control in inbred, H-2 congenic and intra-H-2 recombinant strains of mice. A high response was associated with haplotypes H-2d,a,k and low response with haplotype H-2b. DTH to oxazolone was high or intermediate in different F1 hybrids of high and low responder mice. In F2 and backcross generations a higher response was associated with the "dd", than with "bb" phenotype, while intermediate response was found in the heterozygote "db" mice. A study of H-2 recombinant strains suggests that a gene controlling the DTH response maps in the I-B subregion of the H-2 complex. The response was significantly modified by gene(s) which are not linked to the H-2 complex and have not been mapped. Since congenitally athymic nude (nu/nu) mice did not respond to oxazolone, this contact sensitivity is belived to be a T cell-dependent immune response.

Administration, Topical↗
PubMed1977

Genetic control of two different types of antibody responses to oxazolone.

The genetic control of antibody responses induced by contact sensitization with oxazolone and immunization with an oxazolone-mouse serum albumin conjugate was studied in inbred, H-2 congenic and nude mice. Both types of antibody responses are T cell-dependent and regulated by immune response genes mapping at the I-B subregion of the H-2 complex. The relative magnitude of antibody responses induced by the two methods of immunization is governed by a gene or genes mapping at the I-B subregion of the H-2 complex. Presentation of antigen by these two methods gives H-2-dependent distributions of high and low responsiveness which are exactly opposite. Non-H-2 genes affect the overall level of antibody response but not the relative magnitude of the responses.

Animals↗
PubMed1977

Genetic control of primary and secondary IgG responses to sheep erythrocytes in mice.

The genetic control of the primary and secondary IgG responses to sheep erythrocytes has been studied by using inbred, H-2-congenic, and intra-H-2-recombinant mouse strains. According to our results, the primary IgG respone is under multigenic control. There is a correlation, however, between the titer of primary IgG antibodies produced and the H-2 phenotypes among the mouse strains tested. One H-2-linked gene maps at the I-B subregion, whereas another gene can be mapped at or closely linked to the H-2D region. Low and high responsiveness were associated with H-2b, H-2f and H2a, H-2d, H-2k phenotypes, respectively. By comparison of the responses of inbred and congenic strains having the same H-2 phenotype, it can be concluded that background genes influence the primary response only slightly but have almost complete control over the secondary response.

Animals↗