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L N Fontalin

Publications and source records attributed to L N Fontalin.

At least 55 records · Page 3Linked to original sources
PubMed1980

[Detection of a distinctive differentiating antigen of activated mouse T- and B-lymphocytes--AKA-1].

The presence of a differentiative antigen on activated B cells -- antibody forming cells (AFC), analogous to that against mouse T lymphocytes activated by transplantation antigens was demonstrated with the help of specific rabbit antiserum (ATactS) against these T lymphocytes. The antigen was detectable on direct AFC producing antibodies to sheep, rabbit and rat red blood cells as well as on indirect AFC producing antibodies to sheep red blood cells. The antigen was found on AFC of different H-2 and Ala-1 phenotypes. The activity of ATactS was abolished by absorption with activated T cells, EL-4 lymphoma cells rather than by intact lymphocytes, liver cells, serum or immunoglobulin of mice. The differentiative antigen common to activated T and B cells is proposed to be designated Aka-1.

Animals↗
PubMed1980

[Induction of tolerance to alloantigens in adult mice].

The tolerance to allogeneic C57BL/6 cells (H--2b) was induced in adult CBA mice (H--2k). For tolerance induction three kinds of treatment were combined: thymectomy of adult CBA mice, intravenous inoculation of 1 x 10(8) spleen C57BL/6 cells and injection of 200 mg/kg of cyclophosphamide after 24 hours. Such a treatment of CBA mice resulted in long survival (up to 5 months) of allogeneic C57BL/L heart grafts. The data obtained in MLC reaction supported unresponsiveness of tolerant CBA mice to H-2 antigens of C57BL/6 mice. No lymphoid tissue chimerism was observed in tolerant mice.

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PubMed1979

[Suppression of delayed hypersensitivity in mice receiving a massive dose of xenogeneic erythrocytes].

The injection of 6x109 sheep red blood cells to mice suppresses delayed-type hypersensitivity (DTH) in situ and activates spleen cells which prevent sensitization of recipients. Preliminary thymectomy of donors and the treatment of cell suspensions with anti-T-globulin abolish suppression of DTH. Pretreatment of mice with low doses of cyclophosphamide (CY) enhances antibody formation and DTH. Higher doses of CY increase the DTH reaction but inhibit antibody formation. The data obtained allow to conclude that suppression of DTH is due to the activity of short-living, intensively proliferating cells of thymic origin and possibly to B cells.

Animals↗
PubMed1979

[Induction of immune tolerance to thymus-dependent antigen (sheep erythrocytes) in the absence of T-cells].

The role of T cells in B cell tolerance induction to sheep red blood cells (SRBC) was studied in intact adult mice, in lethally irradiated mice injected with singeneic embryonic liver cells and thymocytes (TB-mice) and in animals functionally deprived of T cells--thymectomized, letally irradiated mice reconstituted with embryonic liver cells only (B-mice). Tolerance was obtained by treatment of mice with SRBC and cyclophosphamide (Cy). Cy-induced tolerance to SRBC was shown to be the result of the absence of specific T cells and partially of immunocompetent B cells. Suppression of immunoreactivity was observed not only in TB-mice but also in B-mice subjected to tolerogenic treatment. Splenocytes of tolerant TB-mice did not suppress the immune response of intact spleen cells to SRBC. The results obtained suggest the conclusion that B cells tolerance could be formed in absence of T cells.

Animals↗
PubMed1979

[Immune response and tolerance to S. typhi Vi-antigen in T-lymphocyte depleted mice].

Comparison of immune response to Vi-antigen in thymetomized letally irradiated and reconstituted with fetal liver cells mice and in control animals revealed no difference between the two groups. The absence of enchancement of antibody formation in T cell depleted mice favours thymic-independent regulation of immune response to optimal dose of Vi-antigen. The induction of cyclophosphamide tolerance to Vi-antigen did not depend on the presence of T cells: tolerogenic treatment was equally effective in T cell depleted mice and in control animals. Therefore cyclophosphamide tolerance was not due to the activation of T suppressors but to direct elimination of immunocompetent clones of B cells.

Animals↗
PubMed1979

[Development of delayed hypersensitivity to sheep erythrocytes after separate and combined administration of the antigen and cyclophosphamide].

The ability to the development of delayed hypersensitivity (DHS) to the appropriate antigen was studied in mice treated with large doses of SRBC and cyclophosphamide at varying time prior to the experiment. Suppression of DHS development induced by administering either the cytostatic alone or a large dose of the antigen was examined at the same periods of time. The combined treatment was shown to induce tolerance according to diverse tests for DHS (skin and macrophage migration inhibition tests). At the basis of this tolerance lies genuine deficiency of the appropriate clone of T cells. Administration of cyclophosphamide alone leads to a slight suppression of DHS, while a large dose of the antigen induces a different form of areactivity due to the suppressor cells whose nature is not yet clear.

Animals↗
PubMed1979

[Effect of thymectomy on induction of immunologic tolerance in the effectors of delayed hypersensitivity].

The influence of thymectomy (Tx) on induction of tolerance of delayed type hypersensitivity effectors (DHE) was examined. Tx did not interfere with induction of tolerance to sheep red blood cells (SRBC) achieved with combined injections of the massive dose of the antigen and cyclophosphamide (Cy). Tx resulted in prolongation of unresponsiveness. The injection of mice with the massive dose of SRBC alone also resulted in tolerance formation. However, this type of tolghtly depressed formation of DHE in intact but not in Cy treated mice. The results obtained are in agreement with the idea of the existence of diverse mechanisms of tolerance induction (clonic-deficient and suppressor). These data also suggest the existence of two subpopulations differing in susceptibility to Cy and Tx in DHE effectors and their precursors.

Animals↗
PubMed1979

[Functional activity of T and B lymphocytes of mice undergoing spontaneous loss of tolerance].

The functional activity of splenocytes and thymocytes of mice tolerant to sheep red blood cells was investigated one and four weeks after tolerance induction. The tolerance was achieved by cyclophosphamide. The immunocompetence of thymocytes was fully reversed in lfour week time. The functional activity of T and B lymphocytes of the spleen was also partially recovered four weeks after tolerance induction. Preliminary thymectomy weakened but did not prevent completely the immunocompetence of T cells of the spleen from being recovered. No Tsuppressants were found in the thymus or spleen of the tolerant animals.

Animals↗
PubMed1979

[Phenomenon of parental resistance and its genetic regulation].

Lymphocytes of mice F1 (CBA X M523) and F1 (A X M523) transplanted to 1000 R irradiated CBA or A mice responded to the test antigens--SRBC or S. typhi Vi-antigen--by formation of 100--1000 times less antibody forming cells than in syngeneic recipients. An intermediate result is achieved when the lymphoid cells are transplanted to the irradiated M523 mice. Lymphocytes of mice F1 (A X CBA), F1 (CBA X C57Bl/6), or F1 (A X A.CA) developed a similar immune response in the irradiated syngeneic mice and in both parental lines. The ability of parental line M523 to respond to SRBC was the same as in the other lines studied when examined in situ or in adoptive transfer experiments. The stem hemopoietic cells of mice F1 (CBA X M523) develop in the spleen of CBA mice 2--2.5 times less hemopoietic colonies than in the spleen of syngeneic animals. A conclusion was drawn that mutation M523 in CBA mice inhibited the proliferation and differentiation of hemopoietic and lymphoid cells in the irradiated nonsyngeneic recipients.

Animals↗
PubMed1979

[Parental resistance of irradiated mice (CBA X M523)F1 to lymphocytes: fate of transplanted cells, duration of resistance and its specificity].

The immune response of (CBA X M523)F1 mouse lymphocytes to the antigen (sheep red blood cells) in CBA mice after lethal irradiation was studied. When irradiation, cell transfer and antigen test-injection were performed at the same day the graft activity was inhibited, in comparison with syngeneic system. The activity of donor cells restored on increasing the interval between these processes up to 3 days. Retransplantation of the spleen cells from recipients to irradiated CBA and F1 mice revealed viability of transplanted cells and lack of their readaptation to insyngeneic microenvironment. The recipient's resistance could be specifically overcome by the preinjection of mouse cells combined with cyclophosphamide or without it. The results obtained allow a conclusion that genetic parental resistance of CBA mice to F1 mouse cells is due to the recipient immunocompetent cells which are inactivated 3 days following irradiation. They do not produce cytotoxic effects with respect to donor cells, blocking, however, their activity for some time.

Animals↗
PubMed1978

[Status of T- and B-lymphocytes in long living CBA--F1 (CBA X C57BL/6) chimeras].

Semiallogeneic chimeras were produced by injecting 3 X 10(7) spleen cells of mice CBA (H--2k, Mlsd) to lethally irradiated mice (CBA X C57BL/6)F1. Two days later recipients were given cyclophosphamide (CP), 2 mg per mouse, to prevent death of graft versus host reaction (GVHR). For 1.5--2 months after the creation of chimerism in 23 of 26 mice under study all cells producing antibodies to SRBC were represented by donor cells of H-2 phenotype; 3 mice were partial chimeras. Spontaneous blast transformation in the cultures of chimera spleen did not exceed the control level, and in the mixed lymphocyte culture chimera cells failed to proliferate on addition of irradiated lymphocytes (CBA X C57BL/6) F1. At the same time chimera gave intensive blast transformation to the irradiated lymphocytes of the third line of mice DBA/2 (H--2d, Mlsa). Among the chimera spleen cells no killers capable of destroying target cells of donor or recipient origin were revealed. Similar results were obtained in vivo: chimera cells gave no positive local GVHR after administration to mice (CBA X C57BL/6) F1. Prolonged chimerism was accompanied by a reactivity of donor T-lymphocytes to the recipient transplantation antigens. A blocking factor was revealed in the blood serum of chimeras. The substitution of donor lymphocytes for the recipient cells begins after 3 to 5 months. At the same period donor T-cell population reconstitutes partially the responsiveness to the recipient antigens and the blocking factor disappears from chimeras blood.

Animals↗
PubMed1978

[Effect of preliminary administration of allogenic cells on transplantation immunity in mice receiving cyclophosphamide].

It was shown that injection of 1 X 10(8) spleen cells from C57Bl/6 mice to CBA mice one day before the injection of cyclophosphamide (CY) helped the take of 2 X 10(7) allogeneic or semiallogeneic cells (injected for the second time 3 to 6 hours after C)). Criterion of survival is the ability of the donor cells to produce antibodies to sheep red blood cells in the recipients tolerant of this antigen. Injection of 1 X 10(8) allogeneic cells two days before CY produces no protective effect. Killer-cells proved to appear on the second day after the immunization with allogeneic cells; their peak was reached on the 5th day. The data obtained suggest that CY eliminated the recipients' lymphocytes, which responded to the transplantation antigens, whereas the killer-cells already formed were stable to the CY action.

Animals↗
PubMed1977

[Mechanism of tolerance to VI-antigen of Salmonella typhi induced by cyclophosphane].

High dose Vi-antigen treatment and injection of cyclophosphamide 46 to 48 hours later induced in mice a state of immunological unresponsiveness remaining stable in adoptive transfer. Only low amounts of the antigen were revealed in the blood and spleen of tolerant animals 2 to 3 weeks after the tolerogenic treatment. No T-suppressors were found in the spleen of tolerant mice--the cells of tolerant mice failed to suppress the immune response of normal lymphocytes when transferred together to the irradiated recipients, or to induce tolerance in normal mice. Normal spleen cells restored partially the immune responsiveness in tolerant animals. The results obtained suggest that cyclophosphamide tolerance was due to deletion or the long-term inactivation of the immunocompetent cells.

Animals↗
PubMed1977

[Primary and secondary immune response in animals following spontaneous loss of tolerance].

Mice subjected to tolerogenic treatment by sheep red blood cells (SRBC) and cyclophosphamide were immunized at various intervals (from 1 to 8 weeks after treatment) either by a single injection of 5 X 10(8) SRBC or by a double-injection of 1 X 10(6) SRBC. In control mice both immunization methods proved to be equally successful. In the experimental animals the immunological memory formation and/or its realization was destroyed to a greater extent and was restored more slowly than the capacity to the primary response.

Animals↗
PubMed1976

[Immunologic competence of T- and B-lymphocytes in tolerance induced by cyclophosphamide].

A study was made of immunological competence of T- and B-lymphocytes of mice subjected to tolerogenic treatment (administration of a massive dose of sheep erythrocytes and cyclophosphamide 7 days before the experiment). The capacity of lymphocytes of tolerant mice to influence the interaction of normal T- and B-lymphocytes was also investigated. This form of tolerance was caused not by T-suppressors, but by a true deficiency of T-cells-helpers (both in the thymus and in the spleen), and partially of B-cells (in the spleen). Some lack of B-cells in the bone marrow was connected with a nonspecific action of cyclophosphamide. Cyclophosphamide is supposed to selectively eliminate cells proliferating in response to the antigen.

Animals↗
PubMed1976

[Relationship between T- and B-lymphocyte cooperation and their syngeneity].

Cooperation efficiency of (CBA x C57BL/6) F1 thymocytes and CBA bone marrow cells in immune response to SRBC was compared with the syngenic combination of the same cells. Selectivity of interaction of the T- and B-lymphocytes of different origin was studied in incomplete cyclophosphamines (CBA x C57BL/6) leads to CBA chimerae, where donors were primed with SRBC and the recipients were either intact or tolerant to the given antigen. F1 T-cells proved to interact with the CAB-B-cells 10-15 times less effectively than with the syngenic B-cells. It is suggested that similarity between the antigenic structure of the cell membrane of the T- and B-lymphocytes, aiding their physical contact, increased the action efficiency of the T-mediator on the B-cell.

Animals↗
PubMed1976

[Factors determining prolonged chimerism of lymphoid tissue in mice treated with cyclophosphamide].

Conditions of long-lasting chimerism induction in adult CBA mice treated with cyclophosphamide and spleen cells (CBAXC57BL/6)F1 were investigated. The necessary requirements are high cell doses (over 50X10(6)), cyclophosphamide dose equal or over 200 mg/kg and a short interval (3-6hr) between their injections. The data obtained were interpreted from the point of view of the capacity of cyclophosphamide to induce reversible lymphocyte DNA damages. After the interaction of lymphocytes with the antigen these damages are fixed with the resultant elimination of the corresponding cell clone.

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