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L N Fontalin

Publications and source records attributed to L N Fontalin.

At least 37 records · Page 2Linked to original sources
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↗
PubMed1985

[Characteristics of the reaction of immunologically tolerant mice to the polyclonal stimulant salmozan].

The nonspecific stimulant of the immune response salmozan (Sal) increases the number of PFC against SRBC in intact mice, B mice (thymectomized, irradiated and reconstituted with embryonic liver cells), and in mice pretreated with cyclophosphamide (CY). This effect was decreased in mice pretreated with SRBC and CY. The subsequent injections of SRBC and Sal into tolerant mice did not increase the response under study. It is concluded that the effect observed is due to partial alteration of antigen-specific B cells of tolerant mice and this alteration cannot be explained by the lack of the regeneration of membrane immunoglobulins.

Adjuvants, Immunologic↗
PubMed1985

Studies on lipopolysaccharide-induced polyclonal B cell activity in mice tolerized by sheep red blood cells and cyclophosphamide.

The polyclonal immune response was induced in untreated mice and mice treated with cyclophosphamide by the administration of lipopolysaccharide from E. coli or S. marcescens. The number of cells forming antibodies to sheep red blood cells and to trinitrophenyl, and of cells producing immunoglobulins increased. The administration of LPS to mice pretreated with SRBC and CY (tolerant mice) considerably reduced the number of anti-SRBC AFC in comparison with the controls. The tolerogenic treatment did not change the number of anti-TNP AFC and IPC. Analogous results were obtained in genetically athymic (nude) mice and in B mice (thymectomized, lethally irradiated and reconstituted with embryonic liver cells). The results suggest that a deletion or a temporary inactivation of a fraction of the antigen-specific B cells occurs in tolerant mice. This inactivation cannot be explained by the absence of expression of surface immunoglobulins on B cells nor by the activity of suppressor T cells.

Animals↗
PubMed1984

Expression of the differentiation antigen of activated T and B lymphocytes (ACA-1) on cells of lymphoid and nonlymphoid tumors.

In cytotoxicity and indirect immunofluorescence tests an antiserum to ACA-1 (activated cell antigen) reacted with 58-100% of actively proliferating cells from tumors of lymphoid (EL-4 T lymphoma, MOPC 104E plasmacytoma) and nonlymphoid origin (AH-22 hepatoma, Sa-1 and MCh-11 sarcomas, F2 mammary cancer). Absorption of anti-ACA-1 serum with tumor cells sharply reduced its activity both against the cells of all these neoplasms and against normal activated T and B lymphocytes. Absorption with proliferating murine cells from the brain of embryos and the retina of neonates or with similar (nonproliferating) cells from adult mice did not affect the activity of the antiserum. It is concluded that ACA-1 is expressed on actively proliferating cells of the tumors studied.

Animals↗
PubMed1984

Immunological status of mice with long-standing allogeneic or xenogeneic neonatal heart grafts.

Adult mice were thymectomized and given 1 X 10(8) allogeneic or xenogeneic spleen cells i.v. On the day following cell injection, the mice were treated with 200 mg/kg cyclophosphamide (Cy) i.p. Of the CBA mice treated according to this protocol, 87% accepted heterotopically transplanted C57BL/6 neonatal heart grafts and 61% accepted August rat heart grafts. Electrical activity of the grafts could be recorded in the majority of recipients for more than 5 months. Graft acceptance in most cases was specific. Some recipients with long standing rat heart grafts produced antirat hemagglutinins, but were negative for lymphocytotoxins. The absence of xenoantibodies correlated with specific unresponsiveness in the mixed lymphocyte culture (MLC) response.

Animals↗
PubMed1984

Blocking activity of the serum from semiallogeneic chimaeras produced by means of cyclophosphamide.

Blocking activity of the serum from semiallogeneic chimaeras produced by the i.p. injection of cyclophosphamide, followed by the i.v. injection of 10(8) spleen cells from (CBA X C57B-L/6)F1 hybrid mice into CBA mice, was investigated. The chimaera serum was found to inhibit local GVHR when injected together with lymphocytes from CBA mice into (CBA X C57BL/6)F1 hybrid mice, but not (CBA X BALB/c)F1 hybrids. Previous absorption of the chimaera serum with C57BL/6 lymphocytes reduced its blocking activity in local GVHR. Absorption with activated CBA anti-C57BL/6 lymphocytes had no effect on blocking activity of the serum. In some experiments the chimaera serum inhibited cytotoxic activity of CBA anti-C57BL/6 and BALB/c anti-C57BL/6 lymphocytes on the corresponding target cells in vitro. Graft-versus-graft reaction of CBA thymocytes against spleen cells from (CBA X C57BL/6)F1 hybrid mice was considerably reduced when irradiated chimaeras were the recipients. Intravenous injection of the chimaera serum into the intact CBA mice did not prolong the survival of C57BL/6 skin allografts. It is concluded that the serum blocking factor is an antibody to the transplantation antigen or an antigen-antibody complex.

Animals↗
PubMed1984

Specific reduction of the immune response to sheep red blood cells by the injection of syngeneic globulin on a non-immunogenic carrier.

Inoculation of normal (CBA X C57BL/6)F1 mice with syngeneic, cellulose-conjugated serum globulin containing anti-SRBC antibodies (anti-SRBC Ig-cel) induced a specific reduction of the immune response to SRBC. This was observed in situ as well as in the adoptive transfer experiments. In the latter case, the animals injected with cellulose-conjugated globulin were the donors of lymphocytes. Furthermore, it was found that the serum from mice injected with an anti-SRBC Ig-cel complex contained anti-idiotype antibodies which inhibited the syngeneic and, to a smaller degree, the parental anti-SRBC antibody-forming cells and had no effect on AFC of some other strains. The formation of anti-idiotype antibodies was T-dependent because these antibodies were produced by T-B mice but not by B mice. We assume that the observed reduction of the immune response to SRBC in vivo was due to the anti-idiotype response to a previous injection of cellulose-conjugated idiotype-positive anti-SRBC antibodies.

Animals↗
PubMed1984

[Delayed hypersensitivity reaction to alloantigens in mice].

A new scheme of induction of delayed hypersensitivity (DH) to alloantigens in mice is described. The optimal conditions for DH development are intraperitoneal injection of 1 X 10(7) cells of the allogeneic spleen to normal mice (not treated with cyclophosphamide) 5 days before the challenge with 5 X 10(6) spleen cells. s.c. The maximal response was seen 24 h after resolution. The reaction was specific, being mediated by T lymphocytes; it could not be transferred to intact recipients by allogeneic serum. However, DH was found to be transferrable by s.c. injection of 5 X 10(6) lymphocytes from sensitized donors. Such a modification of the scheme of DH induction may appear useful for studies of the animals' immunity, particularly for studies of the tolerance to allografts.

Animals↗
PubMed1983

ACA-1, a new differentiation antigen of activated lymphoid cells.

Rabbits were immunized with murine CBA T lymphocytes activated with C57BL/6 antigens (Tact). The immune rabbit sera were adsorbed with murine erythrocytes, serum, liver cells, and unstimulated T and B lymphocytes. Upon absorption, the antisera (ATactS) were not cytotoxic for unactivated thymus, lymph node, and spleen cells of different mouse strains in the cytotoxicity assay. ATactS did not inhibit the immune response of lymphocytes from unimmunized animals to SRBC or their proliferation in mixed lymphocyte culture. At the same time ATactS lysed 67% of actively proliferating T-lymphoma EL-4 cells, 31-56% of the T lymphocytes stimulated with allogeneic cells, and 53-56% of Con A- or LPS-stimulated splenocytes. ATactS also inhibited 90-100% of antigen-activated B cells, i.e., plaque-forming cells (PFC) producing 19 S and 7 S antibodies to serologically noncrossreacting antigens, such as sheep, rabbit, and rat RBC. It also decreased the intensity of the secondary immune response to SRBC. The effect of ATactS did not depend on the H-2 or Ala-I phenotype of target cells. Our experiments showed that ATactS activity fell after absorption with activated, but not quiescent lymphoid cells. These results suggest the presence of a special antigenic marker on activated murine T and B cells which differs from the generally recognized cell surface antigens, such as H-2, Ig, Ala-I, idiotype, Thy-I, MBLA, MTLA, Lyt-1,2,3, and others. It has been designated Aca-I (activated cell antigen).

Animals↗
PubMed1983

[Thymus-dependence of genetic resistance to (CBA x M523)F1 lymphocytes].

The nature of cells responsible for the genetic resistance of lethally irradiated CBA mice to lymphocytes of (CBA x M523)F1 hybrids was studied. Preirradiation of the hosts was shown to abolish the resistance. The latter was generally recovered by syngeneic thymocytes or splenocytes while embryonic liver and bone marrow cells or splenocytes treated with anti-Thy-I serum plus complement before injection into host were ineffective. It is postulated that some cells with T cell characteristics are responsible for the phenomenon of parental resistance. These cells differ in several respects from T cells that mediate the transplantation immunity and from M cells that control other forms of the genetic resistance.

Animals↗
PubMed1983

[A reactivity to polyclonal stimulation of immunogenesis with salmozan after its repeated administration].

The injection of 100 micrograms of salmozan (polysaccharide isolated from Salmonella typhi somatic O-antigen) or 50 micrograms of Escherichia coli lipopolysaccharide into mice induced a considerable increase in the number of antibody-forming cells in the spleen in response to the injection of sheep red blood cells (SRBC) 2-3 days later. This polyclonal effect was essentially weaker if the animals previously received 500 micrograms of salmozan (9-10 days prior to the injection of SRBC). The absence of reactivity was not linked with antibodies to salmozan or with some other serum factor. The lymphocytes of nonreactive mice proved to be capable of polyclonal response in the adoptive system, and at the same time the polyclonal response of intact lymphocytes to salmozan in the body of nonreactive irradiated mice was essentially weakened. The features making the above phenomenon similar to, as well as different from, the so-called "endotoxin tolerance" are analyzed.

Animals↗
PubMed1981

[Regulation of the intensity of delayed-type hypersensitivity to sheep erythrocytes by the K-region of the major histocompatibility complex in mice].

The injection of 6 x 10(9) sheep red blood cells (SRBC) to mice suppressed the delayed type hypersensitivity (DTH) in situ and activated spleen T cells which prevent sensitization of syngeneic recipients. Similar effect was obtained when suppressor cells induced in F1 hybrids were transferred to parental mice. Suppression was also reached in allogeneic strain combination if suppressor cells of donors and recipients shared the major histocompatibility complex (MHC). Studied performed with recombinant and mutant strains revealed that the prerequisite for interaction of DTH suppressors and effectors was the identity of K-region of MHC. Passive transfer of DTH to SRBC was also possible if donors and recipients were identical in K-region of MHC. It is believed that interaction between DTH suppressors and effectors is restricted by a region of MHC whose product takes part in antigen representation.

Animals↗
PubMed1980

Mechanisms of antigen-induced blockade of immune response and cyclophosphamide-promoted tolerance to Salmonella typhi Vi antigen.

Blockade of the immune response, caused by a high dose of Salmonella typhi Vi antigen (200 microgram i.v.) and cyclophosphamide (CY)-induced tolerance to Vi antigen, were analyzed. The results of the study show that blockade of the immune response cannot be attributed to masking of the response resulting from neutralization of antibodies by the excess of non-cell-bound antigen. A high dose of Vi-antigen induced triggering and proliferation of specific B precursors but reversibly suppressed synthesis or secretion of antibody by plaque-forming cells. A single injection of CY (200 mg/kg i.p.) 2 days after a high dose of Vi antigen markedly prolonged the antigen-induced state of unresponsiveness. CY-induced tolerance to Vi antigen is due to elimination or long-term inactivation of specific B precursors. Dissimilarities in the characteristics of immune response blockade and CY-induced tolerance are discussed as well as their possible implications for the mode of action of CY.

Animals↗
PubMed1980

Genetic resistance of CBA and A mice to transplanted lymphoid and hemopoietic cells of CBA.M523 mutants and their F1 hybrids.

(CBA X M523)F1, (A X M523)F1 and M523 lymphocytes grafted into lethally irradiated CBA or A mice temporarily lose their capacity to respond to test antigens (SRBC, Vi-antigen, S. typhi). Immunoresponsiveness of F1 cells is affected to a lesser degree in lethally irradiated M523 mice. Depression of response is absent in the CBA leads to F1 combination, in the syngeneic combination and in CBA mice whch have received transplanted cells from F1 hybrids which do not share the M523 mutation. The number of hemopoietic (CBA X M523)F1 colonies was also reduced in CBA mice. Resistance of CBA mice to lymphoid (CBA X M523)F1 cells develops 18 days after birth. It can be reduced by additional recipient preirradiation or preinoculation with (CBA X M523)F1 spleen cells. The abrogated resistance can be partially restored by CBA spleen cells. The activity of (CBA X M523)F1 lymphocytes passaged through CBA spleen is restored in syngeneic F1 secondary recipients but inhibited again in the CBA secondary recipients. These results are consistent with the suggestion that resistance of lethally irradiated CBA mice to hemopoietic and lymphoid (CBA X M523)F1 cells is mediated by immunologically competent, radioresistant recipient cells rapidly reacting to transplantation antigens coded by the mutant H-2Kka allele. These cells temporarily suppress the functional activity of transplanted cells but do not eliminate them.

Animals↗
PubMed1980

Tolerance to allogeneic and to xenogeneic heart grafts provided by thymectomy of adult mice combined with donor cell and cyclophosphamide inoculation.

A new method of induction of tolerance to allogeneic and to xenogeneic cells is presented. It includes thymectomy of adult mice followed 1 month later by the injection of 1 X 10(8) spleen cells i.v. and i.p. administration of 200 mg of cyclophosphamide per kg 1 day after cells. This method induced prolonged survival of heterotopically transplanted neonatal C57BL/6 murine heart grafts (more than 8 months) and of August rat heart grafts (more than 2 months) in CBA mice. Tolerance to allo- or xenoantigens was formed at the cell level. Experimental animals did not produce allo- or xenohemagglutinins after graft implantation. Spleen cells of mice with surviving C57BL/6 heart grafts did not respond to C57BL/6 cells in mixed lymphocyte culture (MLC) reaction. Lymphoid cell chimerism was not observed in animals tolerant to alloantigens.

Animals↗