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L N Fontalin

Publications and source records attributed to L N Fontalin.

At least 19 recordsLinked to original sources
PubMed1992

T-cell immunodeficiency induced by T-cell mitogens combined with cyclophosphamide injection.

In the murine system in vivo administration of several T-cell mitogens (LcA, Con A, anti-Thy 1.2 mAb) followed by cyclophosphamide (CP) inhibited the functional activity of T-cell subsets (Th1, Th2, Ts) but not that of B cells. T-cell counts in the spleen of treated mice proved to be significantly decreased. Conversely, T mitogens or CP alone produced a negligible effect if any. Adoptively transferred thymocytes from intact donors restored T-dependent splenocyte responses in experimental mice. In addition, it did not suppress the normal response to sheep red blood cells (SRBC). Our results indicated that the acquired immune deficiency under study is caused by polyclonal elimination (deletion) of mitogen-stimulated T cells, and could be regarded as a model of CP-induced tolerance.

Animals↗
PubMed1992

[Experimental influenzal and tuberculous infections under conditions of specific and nonspecific immunosuppression].

The course of influenza and tuberculosis infections under the conditions of disturbances in the immune response of experimental animals has been studied. As revealed in the survival test, the induction of secondary T- and B-cell-mediated immunodeficiency in mice leads to an increase in the sensitivity of the body to influenza virus, especially in cases of T-cell-mediated immunodeficiency. The injection of BCG in combination with cyclophosphamide into mice induces tolerance to this antigen in the animals; this tolerance has a "split" character, i.e. it affects only T-cell-mediated, but not humoral immunity. The induction of T-cell-mediated immunodeficiency or tolerance to BCG in mice has been shown (in the survival test) to lead to the development of the sensitivity of the animals to experimental tuberculosis infection. B-cell-mediated immunodeficiency did not influence the animal survival rate.

Animals↗
PubMed1991

Autoimmune response induction and regulation in rat erythrocyte-immunized mice.

The process of antibody formation to self-red blood cells (RBC) has been studied in rat RBC (rRBC)-immunized mice. A positive correlation was noted between antibody production to mouse RBC (mRBC) and rRBC in some mouse strains. The low responsiveness on both indices was overcome by s.c. injections of rRBC in low doses. rRBC-tolerant mice exhibited lower levels of antibody production to mRBC. Splenocytes from rRBC-immunized donors, when transferred to irradiated recipients, revealed enhanced and accelerated anti-mRBC and anti-rRBC antibody production in response to rRBC but not to autologous mRBC. Consequently, the autoimmune process is not accompanied by disordered immunologic tolerance to self-RBC and requires participation of Th responding to foreign epitopes of rRBC antigens. Splenocytes from rRBC-immunized donors, when transferred to non-irradiated recipients, inhibited antibody production to mRBC. The suppressive effect was not abrogated by pretreating donors or recipients with low doses of cyclophosphamide (CP) or by pretreating donors with antibodies to I-J. It was abrogated by the elimination of cells of donor origin within 8-9 days after transfer. Inoculation of antibodies to rRBC in immunized mice on a schedule imitating their splenocyte transfer dynamics inhibited antibody production to mRBC. Therefore, it can be assumed that the suppressive effect of cell transfer is accounted for, not by suppressors or their inducers, but by antibodies to rRBC on the basis of feedback regulation.

Anemia, Hemolytic, Autoimmune↗
PubMed1989

Recovery from polyclonal tolerance: simulation analysis.

Mathematical model of immunological tolerance was applied to polyclonal B cell tolerance induced in mice by treatment with bacterial lipopolysaccharide (LPS) followed by the application of cyclophosphamide (CY). Satisfactory simulation results were obtained with the life-span of lymphocytes shorter than the experimentally observed one. It could be assumed that the massive decrease of lymphocyte population in polyclonal tolerance would elicit a compensatory reaction. Therefore it was postulated that some kind of feedback mechanism increased the influx of B lymphocytes. Having this factor included in the model, satisfactory agreement of the simulation results with experimental data was obtained for experimentally determined life-span of B cells.

Animals↗
PubMed1989

[Antibody formation to autologous erythrocytes following the immunization with rat erythrocytes of normal animals and mice tolerant to the immunizing antigen].

(CBA X C57B1/6)F1 mice immunized three times with rat erythrocytes produced antibodies both to this antigen and to autologous erythrocytes. Most of the antibodies to rat erythrocytes belonged to IgM isotype while antibodies to autologous red cells were of IgG isotype. Combined injection of thymectomized (CBA X C57B1/6)F1 mice with a massive dose of rat spleen cells and cyclophosphamide induced in animals stable tolerance to rat cells. Inducibility of antibodies to autologous red cells in tolerant mice injected 3-5 times with rat erythrocytes was drastically reduced. Nonspecific suppression (thymectomy and cyclophosphamide) did not prevent production of autoantibodies.

Animals↗
PubMed1988

[Suppressors of the graft vs graft reaction in tolerance to alloantigens].

Immune response and suppressor cell activity of CBA (H-2k) mice made tolerant to allogeneic C57B1/6 (H-2b) heart graft were studied in graft-versus-graft reaction (GvGR). Intact CBA spleen cells inhibited response of (CBA X C57B1/6)F1 cells to antigenic stimulus (sheep red blood cells--SRBC), when injected together into lethally irradiated (CBA X C57B1/6)F1 mice. Spleen cells of tolerant mice were unable to decrease immune response of (CBA X C57B1/6F1 lymphocytes to SRBC and suppressed specifically the inhibition induced by intact CBA spleen cells. Spleen cells from tolerant mice were also capable of suppressing GvGR induced by CBA lymphocytes immune to C57B1/6 cells. Pretreatment of tolerant spleen cells with rabbit antithymocyte globulin and complement before adoptive transfer diminished markedly the suppression. The results obtained in the study suggest that suppression of transplantation immunity in this model is mostly due to T suppressor cells.

Animals↗
PubMed1988

[T-cell immunodeficiency in mice receiving lectin and cyclophosphamide].

Cyclophosphamide injections to mice following T cell mitogen (lectins from Lens culinaris and concanavalin A) were shown to suppress (20-40-fold) thymus-dependent response to SRBC. At the same time no damage-specific and polyclonal response to thymus-independent antigen and polyclonal activator of B cells--lipopolysaccharide--has been observed. Injections of lectin and cyclophosphamide to mice prevented the onset of DTH reaction to SRBC and induction of antigen-specific DTH suppressor cells. Thus, cyclophosphamide injection after T cell mitogen leads to T-cell anergy, with B-cell activity remaining unchanged.

Animals↗
PubMed1988

[The nature of immunodeficiency induced by injections of lectins and cyclophosphamide].

Consecutive injections of T-cell mitogen (LcA, Con A) and cyclophosphamide (CY) produce an inhibition of T-cell, but not B-cell functions. This phenomenon was not a result of suppressor-cell activity of the action of some suppressor serum factors. Immunoreactivity of mice, treated with Con A CY is restored by thymocytes from intact donors, but not bone marrow cells. Using, monoclonal antibodies to Thy-1.2 antigen or anti-Ig serum it has been shown that pretreatment of mice with lectin and CY resulted in a decrease in T-cell, but not B-cell number in comparison with control mice. The above facts are indicative of CY-mediated elimination of T cells involved in proliferation and differentiation by lectin.

Animals↗
PubMed1988

Polyclonal B cell anergy induced by bacterial lipopolysaccharide and cyclophosphamide.

Tolerogenic treatment of mice by successive injections of lipopolysaccharide (LPS) from E. coli or S. marcescens and cyclophosphamide (CY) decreased both the specific and polyclonal responses to tolerogen and to irrelevant LPS from Br. abortus as well as the specific immune response to sheep red blood cells. Splenocytes of tolerant mice were unresponsive to polyclonal challenge when transferred to irradiated syngeneic recipients. Spleen cells or blood serum from tolerant mice did not suppress the polyclonal response of intact mice to LPS. Possible reasons for the polyclonal B cell anergy were analyzed.

Animals↗
PubMed1988

[Tolerance to a xenotransplant in an adoptive system].

Splenocytes of mice tolerant to rat neonatal heart graft were unable to respond to rat blood cells (RBC) when transferred adoptively to lethally irradiated syngeneic recipients 10 or 30 days after tolerogenic treatment. Early after induction of tolerance spleen cells of experimental mice were also unable to respond to sheep red blood cells. However, they responded vigorously to goose red blood cells. Later on (30 days after treatment) tolerance was found to be strictly RBC-specific. Cells suppressing anti-RBC response of intact cells were detected in the spleen of mice both 10 and 30 days after the induction of tolerance. Their suppressive activity was strictly RBC-specific. The results obtained show that early after tolerogenic treatment experimental mice are unable to respond due both to the deficiency of T-helpers involved in the response to mammalian blood cells and to activation of RBC-specific I-J+ T-suppressors. Thirty days after treatment tolerance is maintained solely by RBC-specific T-suppressor cells.

Animals↗
PubMed1987

[Mechanisms of polyclonal tolerance induced by lipopolysaccharide and cyclophosphamide].

The treatment of recipient mice with LPS from S. marcescens followed by the injection of CY 48 h later inhibited a subsequent antibody production against unrelated antigen (SRBC) and polyclonal mitogen (LPS from Br. abortus). Such a reactivity persisted for 2-3 weeks after treatment. It was shown that the number of Ig+ cells in the spleens of treated mice was decreased, while the population of spleen Thy-1.2+ cells remained unaltered. Cell-cooperative test revealed that the function of B cells, but not T cells, was inhibited by the treatment. There were no changes in DTH response to SRBC. Thus, a subsequent treatment of mice with LPS and CY led to B-cell deficiency. The nature of this phenomenon is presumably the same as the nature of CY-induced antigen-specific immunological tolerance.

Animals↗
PubMed1987

[Delayed-type hypersensitivity to minor histocompatibility antigens and its genetic restriction].

The analysis of skin allograft survival time and the level of delayed-type hypersensitivity (DTH) reaction to major and minor histocompatibility antigens revealed the correlation between these parameters of the transplantation immunity. The data obtained have shown that histocompatibility in several non-H-2 antigens induces DTH reaction comparable with the reaction caused by H-2 antigens. The effector phase of DTH to non-H-2 antigens is H-2 restricted. No restriction of the afferent phase is revealed. The application of these results to the analysis of the mechanisms of the recognition of minor histocompatibility antigens in DTH is discussed.

Animals↗
PubMed1986

[Protective role of effectors and T-suppressors of delayed hypersensitivity in mice with a localized staphylococcal infection].

To induce delayed hypersensitivity (DH) in mice, experimental local infection with a small dose of Staphylococcus aureus was used. The production of suppressor cells was shown to occur after the intravenous injection of a large dose of killed staphylococcal culture. Experiments with the use of cell transfer and the treatment of lymphocytes with Thy-1 antiserum in the presence of the complement demonstrated the T-lymphocytic nature of DH and its suppression. The study revealed that the role played by DH in antistaphylococcal immunity was different in the animals infected by the subcutaneous routes; besides, the regulatory action of T-suppressors of DH was established.

Animals↗
PubMed1985

[Immune response and immune tolerance to the O-antigen of Shigella flexneri VI].

The method for the determination of the number of cells synthetizing antibodies to S. flexneri VI O-antigen in the spleen of mice has been developed. Primary immune response to this antigen has been studied with the use of the new method. Immune response to the optimum immunogenic dose of O-antigen has a manifest variable character. The intensity of primary immune response has been shown to rise with the increase of the dose of O-antigen from 0.004 to 50 micrograms. The preliminary injection of 200 micrograms of O-antigen, followed by the injection of cyclophosphamide 2 days later, leads to the development of specific immunological tolerance to O-antigen in experimental animals.

Animals↗