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T K Novikova

Publications and source records attributed to T K Novikova.

At least 19 recordsLinked to original sources
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).

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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