[Changes in the number of neuromediator receptors on murine lymphocytes in ontogeny].

It has being shown by radiological methods of evaluation of the binding sites with adrenergic, cholinergic and neuropeptide agents that during mice ontogenesis the number of binding sites to these agents is progressively declined. The cAMP accumulation by lymphoid cells after contact with adrenaline is declined also. The regularities shown may reflect processes of the immune change during the age.

[The effect of proteolytic cleavage of potato virus X coat protein on its ability to self-assemble with RNA and viral infectivity].

The process of proteolytic cleavage of potato virus X coat protein molecules inside the virions and in the dissociated state in the course of their purification and storage has been studied. In agreement with the previous reports, the intact form (Ps) of the coat protein in the viral particles was found to be gradually cleaved to three discrete lower molecular forms (Pi, Pf, Pu). During the storage of the dissociated coat protein preparations further cleavage was observed with formation of at least three additional lower molecular weight forms (Ppa, Ppb, Ppc).

[Effect of preparations on the intracellular cAMP and prostaglandin E content and on the functional activity of antigen-induced B-suppressors].

Not adhering to a plastic, B-cells of intact or immunized with the suboptimal dose of ram erythrocytes mice were treated in vitro with several agonists and antagonists of cAMP and prostaglandins E and then were transferred to syngenic or allogenic unirradiated recipients. Afterwards the number of the antibody-forming cells against ram erythrocytes was determined. It was shown that a decrease of cAMP and prostaglandin E contents in the intact B-cells results in the appearance of the ability to stimulate the immune response.

[Difference in the mechanism of self-assembly in vitro in tobacco mosaic virus and potato virus X].

The effects of 254 nm UV-irradiation of tobacco mosaic virus (TMV) and potato virus X (PVX) RNA preparations on the RNA ability to self-assembly in vitro with the viral coat proteins were studied. It was found that while TMV RNA ability to assemble with the homologous protein is rapidly inactivated by the UV-irradiation, PVX RNA ability to be encapsidated by the PVX coat protein is quite resistant to the irradiation. More than that, the irradiation of TMV RNA with the dose strongly inhibiting its assembly with the homologous protein, did not result in any significant inhibition of this RNA ability to be coated with the PVX protein.

[Effect of aminoxidase activity regulators on the humoral immune response and proliferation of lymphoid and nonlymphoid cells].

DL-malic acid dibenzylhydrazide (I) and dihydrazide (II), inhibitors of aminoxidases, have been shown to inhibit immune reactions when administered at the phase of initiation but to stimulate the immune response and proliferation of lymphoid and nonlymphoid cells if given on the 2nd and 3rd day following immunization when the immune reaction is in progress. The intensity of local allergic reaction during passive skin anaphylaxis is reduced by I and enhanced by II if the compounds are administered 16 hrs prior to antigen challenge.

[Effect of antiglobulin serum on the expression of M-cholinoreceptors of spleen lymphocytes of intact and immunized mice].

Using a labelled blocker of M-cholinoreceptors (M-CR)--3H-Quinuclidinyl benzilate--the number of the receptors on spleen lymphocytes has been determined before and after immunization of CBA and BALB/c mice with antiglobulin serum. The incubation of non-separated spleen cell suspension with antiglobulin serum decreased the number of M-CR by 14%, while the incubation of the enriched B-lymphocyte suspension decreased it by 32.5%.

[M-cholinergic receptors of B-lymphocytes during immune response in mice].

The number of M-cholinergic receptors on spleen B-lymphocytes of CBA mice was determined using radioactive blocker 3H-Quinuclidinil benzilate. 3 and 4 days after the animals' immunization with ovalbumin the number of M-cholinergic receptors somewhat increased. Specific antigen attenuated M-cholinergic receptor expression on B-lymphocytes, most pronounced on day 4 after immunization, without affecting the receptor expression in control animals.

[Effect of cholino- and adrenomimetic substances on B-lymphocyte proliferation in mice during a primary immune response to a protein antigen].

A study was made of the effects of the neurotransmitters acetylcholine and adrenaline on proliferation of B lymphocytes of mice immunized with ovalbumin. The neurotransmitters were noticed to be capable of changing B cell proliferation on cultivation in vitro. The effect (an increase or reduction of 3H-thymidine incorporation) depended on the time of immunization, antigen dose, and the type of a neurotransmitter.

[Regulation of the cell cycle of B-lymphocytes in mice by substances elevating the levels of intracellular cAMP and cGMP].

Spontaneous velocity sedimentation of B lymphocytes activated by intraperitoneal injection of ovalbumin into mice was used to obtain cell cycle synchronized cells, evidenced by differences in the incorporation of labeled precursors of protein and nucleic synthesis (14C-methionine and 3H-thymidine). The effects of acetylcholine and adrenaline, cAMP and cGMP on the intensity of 3H-thymidine incorporation into mouse B lymphocytes and on the amount of the cells entering mitosis were examined. It was shown that acetylcholine is capable of stimulating whereas adrenaline of inhibitin B lymphocyte entry into the stage of DNA synthesis and egress of these cells from the stage of DNA synthesis to the stage of mitosis.

[Suppressor activity changes in human T-lymphocytes as affected by adreno- and cholinotropic substances].

The influence of oxyfedrine (beta-adrenoagonist) and carbocholine (cholinoagonist) on the functional activity of Con A-induced suppressor T-lymphocytes in healthy persons and in bronchial asthma patients was studied. Oxyfedrine at a concentration of 10 micrograms/ml (10(-5) M) was shown to induce a significant increase in the suppressing activity of both normal lymphocytes and those obtained from bronchial asthma patients. The repeated incubation of lymphocytes with carbocholine at a concentration of 5 micrograms/ml (10(-6) M) led to the removal of the suppressing effect of normal lymphocytes and to the increase of the activating effect of lymphocytes from bronchiae asthma patients.

[Acetylcholine-induced lymphocyte mobility in intact and sensitized mice].

During sensitization of BALB/c mice to protein antigen, spontaneous and acetylcholine-induced mobility of spleen lymphocytes increased, the maximum being reached on days 1-3 from the sensitization commencement. The acetylcholine-induced mobility of lymphocytes was reduced if the lymphocytes had been preexposed to the antigen. The data obtained attest to the same cellular substrate of antigen and acetylcholine effects.

[Antibody-forming cells in rat spleen following midbrain injury].

The number of plaque-forming cells (PFC) in the spleen of rats immunized with sheep red blood cells after the injury of the anterior or the posterior portions of the medial hypothalamus, and also of the thalamus displayed no significant difference from the number of PFC in the spleen of intact animals. The titres of hemolysing and hemagglutinating antibodies in the animals with injuries of the mid-brain were somewhat lower than in the intact animals. A reduction of the circularing antibodies level was not associated with localization of the foci of injury and apparently served as the sequence of the craniocerebral trauma.

[Effect of bilateral destruction of the structures of the medial hypothalamus on the course of anaphylactic shock].

Anaphylactic shock induced in rabbits by the preliminary injury of various areas of the medial hypothalamus coursed more severly than in control. Irrespective of the localization of the foci of injury a more pronounced hypotensive reaction and a slower compensatory elevation of the blood pressure occurred in response to the administration of the reactive dose of the antigen. The severity of anaphylactic shock depended on the time lapse from the moment of hypothalamic injury to the moment of administration of the reactive dose of the antigen.