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Biomedical subjects

A M Moroz

Publications and source records attributed to A M Moroz.

At least 19 recordsLinked to original sources
PubMed1991

[Production of immune interferon in experimental tuberculosis and antituberculosis vaccination in mice].

The serum content of interferon (IF) and its correlation with diverse immunologic parameters were studied in tuberculosis-resistant mice. In primary contamination the IF level was much higher in B10 mice highly sensitive to tuberculosis infection in all periods of the study than that in highly resistant A/Sn mice. In the vaccinated mice which were later infected this tendency remained but IF levels were 1.5--2 times higher than in primary contamination. Comparison of the IF level and the studied resistance parameters in the resistant mice revealed an inverse correlation. If the immunologic parameters in resistant A/Sn mice are higher than those in B10 mice the latter have significantly higher serum IF levels.

Animals↗
PubMed1991

Regulation of T-cell proliferative responses by cells from solid lung tissue of M. tuberculosis-infected mice.

We have studied proliferative responses to mycobacterial antigen preparation (PPD) and to non-specific stimuli of interstitial cells from the lungs of Mycobacterium tuberculosis-infected CBA mice. PPD-reactive lymphocytes appeared in the lung wall tissue in the course of chronic infection, but their proliferative capacity was totally inhibited by the lung macrophages. The latter were also able to suppress the proliferation of immune lymph node T cells. The mechanism of suppression clearly had two components, one being infection-specific and the other non-specific. Non-specific suppression was mediated mainly by prostaglandin E(PGE), whereas the specific mechanism showed only a weak influence of PGE and depended on the presence of I-J+ Lyt-2- nylon-wool-adherent cells in the responder population. Interstitial lung T or B lymphocytes were not involved in specific suppression.

Animals↗
PubMed1990

[New alloantisera to antigenic determinant I--J, their specificity and effect on the course of tuberculous infection in mice].

Preparations of anti-I--J alloantisera with higher activity were obtained by a new method, based on induction of expression of the I--J determinant in donor suppressor cells, immunization of mice with such cells, and subsequent elimination of contaminating anti-idiotypic antibodies from antisera by their adsorption on the cells of the recipient murine strain sharing induced idiotype with the donor cells. After adsorption anti-I--J activity remained unchanged. The antisera thus obtained were found active in the standard cytotoxic assay (working dilution greater than or equal to 1:20). The injection of anti-I--Jk antiserum to CBA mice prolonged the survival time of the animals and increased the parameters of the cell-mediated immunity after infection with Mycobacterium tuberculosis virulent strain H37Rv.

Alleles↗
PubMed1990

[Cellular mechanisms of suppression of T-lymphocyte proliferation by lung cells in experimental tuberculosis].

The ability of interstitial lung cells from mice, infected with Mycobacterium tuberculosis H37Rv, to suppress proliferative responses of immune lymphocytes to mycobacterial (PPD) and unrelated (Staphylococcus aureus cytoplasm) antigens was studied. Two types of suppression were observed: the specific one, which was characteristic of the PPD-response only; and non-specific. The latter was mediated mainly by prostaglandins, since it could be abolished by indomethacin. Both types of suppression depended on the presence of plastic and nylon wool adherent phagocytes from infected lung. Though the depletion of T or B lymphocytes from the lung cell population have not abrogated the suppressive effect, some intercellular interactions were required for antigen-specific suppression, since the presence of nylon wool adherent cells in the population of responder lymph node cells was necessary for its development.

Animals↗
PubMed1990

[Interrelationship between the Bcg and Tbc-1 genes].

The relationship of the mouse Bcg and Tbc-1 genes was studied. It was shown that the F1 hybrids between highly susceptible to tuberculosis mice I/St (Tbc-1s) and the Bcgs-carrying strains were highly resistant to M. tuberculosis H37Rv infection. These results point to complementation of Bcgs and Tbc-1s genes. Analysis of survival time of the [(AKR x B10-fzy)F1 x B10-Fzy]BC1 offspring showed that the mouse chromosome 1 does not regulate resistance to H37Rv infection. No linkage of the Tbc-1s gene with chromosome 1 was revealed when using fzy gene as a marker of the chromosome 1.

Animals↗
PubMed1990

[The genetic regulation of host response to inoculation with Mycobacterium bovis (BCG) and Mycobacterium tuberculosis H37RV].

Vaccination with M. bovis (BCG) essentially prolonged survival time (ST) of several strain mice, with the exception, of CBA/N, infected with M. tuberculosis H37Rv. ST of CBA/N, differing from CBA by xid mutation, was not prolonged by vaccination. Mouse strains with alternative alleles of BCG gene (s and r) and fzy gene as a genetic marker for Bcg5 were used for segregation analysis. It was shown that ST, the level of DTH reaction of mice infected with M. tuberculosis H37Rv, and protective effect of BCG vaccination did not depend on Bcg gene. However, Bcg gene, apparently, regulate the DTH response to PPD in mice only vaccinated with M. bovis (BCG).

Animals↗
PubMed1990

[Suppression of immune response by lung cells in experimental tuberculosis].

In vitro proliferative response of lung cells from mice infected with Mycobacterium tuberculosis H37Rv against PPD and Con A was studied. It was shown that the infected lung contained immune T cells, but their response in vitro was totally inhibited by plastic and nylon wool adherent suppressor cells. The whole population of lung cells from infected, but not intact mice, efficiently suppressed the proliferative response of immune lymph node cells against various antigens (non-specific suppression). The inhibition of response again depended on the presence of plastic adherent lung cells. Our data suggest that at least two suppressor pathways are induced in the course of tuberculosis infection: one being specific for mycobacterial antigens and other non-specific. Both types of suppressor pathways depend on the plastic adherent lung cells from tuberculosis lesion.

Animals↗
PubMed1989

Local adoptive transfer of delayed-type hypersensitivity to tuberculin from M. bovis (BCG) infected mice.

Immunological properties of the cells mediating delayed-type hypersensitvity to tuberculin and genetic requirements of this reaction have been studied by the method of local adoptive transfer. Peritoneal cells from BCG-immunized mice transferred the reaction into unprimed recipients without any genetic restriction. In contrast, nonadherent peritoneal cells transferred the reaction only in H-2-compatible donor-recipient strain combinations. The use of H-2 recombinant strains has shown that delayed-type hypersensitivity to tuberculin in mice is restricted by the I-A locus. Monoclonal antibody against I-Ak beta abrogated (without complement) the transfer of the reaction to CBA recipients. The phenotype of nonadherent cells, transferring the reaction has been shown to be Thy-1+, Lyt-1+, 2-, L3T4+.

Animals↗
PubMed1988

[Genetic restriction of delayed-type hypersensitivity to tuberculin in mice].

An adoptive local transfer method has been used to study the immunological features and genetic restriction of cell interaction during the development of the delayed-type hypersensitivity (DTH) to tuberculin in mice. Peritoneal cells from the BCG-infected mice transfer the DTH to intact animals (into hind footpad) in both syngeneic and allogeneic donor-recipient combinations. Nonadherent cells (macrophage-deleted) transfer the reaction in syngeneic but not allogeneic combination. The use of H-2 recombinant mouse strains demonstrated that successful transfer of the DTH requires I-A subregion compatibility. Treatment of CBA cells with anti-Thy-1.2 antiserum abrogates the reaction transfer. These results indicate that antigen presentation to immune T-cells proliferating during DTH to tuberculin is mediated through the molecular products of the I-A subregion.

Animals↗
PubMed1988

[Regulation of antitubercular immunity in mice by genes of the H-2 complex].

Development of DTH reaction and survival time after M. tuberculosis H37Rv infection have been studied in H-2 congenic and recombinant mice pretreated with high doses of BCG vaccine. In addition, in vitro proliferation of lymphocytes from infected CBA, B6 and 4R mice to PPD was studied in the presence of anti-I-A and anti-I-E mAbs. High doses of BCG vaccination (1 mg/mouse) have led to a significant inhibition of DTH and diminution of survival time in B10.M (H-2f) mice only, and to opposite effects in all other strains tested (H-2a, b, d, k, h4). In I-A+, I-E- 4R mice anti-I-Ak mAbs abrogated lymphocyte proliferation to PPD completely, while in I-A+, I-E- CBA mice only the mixture of anti-I-Ak and anti-I-Ek mAbs was effective.

Animals↗
PubMed1986

[Genetic aspects of experimental tuberculosis in mice].

Susceptibility of inbred mouse strains, their F1 hybrids, offsprings from BC1 and RI strains from CXB pannel to tuberculosis infection was studied. Mice were infected with virulent strain of M. tuberculosis H37Rv. All F1 hybrids, with the exception of (BRSUNT X I/St)F1, showed superresistance, due apparently to heterosis effect; (BRSUNT X I/St)F1 demonstrated an intermediate level of resistance, as compared with parental strains. Analysis of [(BALB/c X B6)F1 X B6]BC1, [(BALB/c X B6)F1 X BALB/c]BC1 offsprings and RI strains indicated that strains BALB/c and B6 have different alleles of at least two genetic loci mediating susceptibility to tuberculosis.

Alleles↗