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With a purpose of identifying and ranking factors influencing remodeling of vascular wall in 168 practically healthy subjects (71 men, 97 women) aged 30-60 years we conducted a study of risk factors of cardiovascular disease, and infectious, immunological, inflammatory and metabolic parameters. Using artificial neural network we found that process of remodeling of vascular wall was most significantly impacted by: cytomegalovirus and hlamydia neumoniae infections, decreased number of T-lymphocytes, development of latent vascular microinflammation, and diastolic blood pressure above 80 mm Hg.

A characteristic feature of systemic autoimmune diseases along with appearance of autoantibodies targeting self-antigenes is deposition of immunoglobulins and components of the complement system in kidneys. However, mechanisms of the deposit formation and their cytotoxic effects still remain poorly studied. To elucidate these questions, we used SJL/J mice which are known to develop autoimmune process accompanied by the appearance of anti-fibrillarin antibodies following regular administrations of sublethal dozes of HgCl2. Using antibodies to the total murine ummunoglobulins we showed that immunodeposits were present in glomeruli of autoimmune and control (not-autoimmune) animals, but their intensity was directly correlated with the titer of anti-fibrillarin autoantibodies and was minimal in control mice. By confocal microscopy and conventional fluorescence microscopy it was defined that immunodeposits deeply penetrate glomeruli and are the most likely located within mesangial cells. In autoimmune animals, ummunoglobulins completely colocolized with the C3--component of complement, but not with the major autoantigen--the protein fibrillarin. We failed to determine the signs of cell proliferation or death in glomeruli. The most prominent difference between control and autoimmune mice was the presence if immunodeposits in renal blood vessels. These observations argue in favor of the idea that destructive and disfunctional renal lesions accompanying development of autoimmune diseases can be caused, in part, by accumulation of immunodeposits in blood vessels.

The appearance of macrophages in arterial wall in early morphogenesis of atherosclerosis was noted by N. N. Anichkov in 1940. The macrophages originate partly from monocytic hematogenous elements, partly from subendothelial cells. The authors show that macrophages of monocytic origin play a leading role in atherogenesis-related complex cellular-molecular alterations in the zone of arterial lesions. A cascade of cellular reactions with participation of macrophages determines a chronic course of the process by type of immune inflammation reactions with autonomic regulation.

The content and tropism of anticerebral antibodies were examined in 20 schizophrenic patients using the indirect immunofluorescence and complement fixation tests. With the aid of the latter the antibodies were revealed in 15 patients, the antibodies to the homologous brain being more frequent in patients with a more severe, continuously progressing schizophrenia, while the antibodies to a heterologous (rat) brain were more often detected in patients with slowly progressing forms of the disease. In 18 patients, the indirect immunofluorescence test showed fixation of immunoglobulins on the nervous tissue components, such as, neurons, myelin, vascular walls. Rather frequently fluorescence of the microglia cells was observed: according to literary data this is not the case with sera of neurological patients. Of attention was a selective fluorescence of the canaliculi observed in examinations of the renal tissue. The data obtained point to a participation of the immunological reactions in the schizophrenia pathogenesis, these reactions involving various morphological and functional systems.

Experiments were conducted on guinea pigs and rabbits. It was shown that treatment of human femoral vessels with metaperiodate and glutaraldehyde solutions led to a sharp (10-fold) reduction of the amount of water-soluble proteins in the tissue homogenates, to a decrease of the sensitising and anaphylactic activity of the extracts, to inertia in the precipitation test with homologous antiserum to crude tissue.

Pecularities attending the fixation of antibodies from the sera of patients with arterial hypertension, amyotrophic lateral sclerosis, multiple sclerosis, hepato-cerebral disease, and myoclonus-epilepsy were studied by the indirect Coons' method. Antibrain antibodies, complimentary to various nervous tissue structures always formed in the patients suffering from the mentioned diseases. The antigenic properties of individual components of the brain tissue of the patients failed to change as much as to differ completely from the antigenic properties of the same formations in normal animals. At the same time various components of different neurons and glial cells, myelin membranes of various conductive systems, and, to a lesser degree, cells of the ependyma and vascular walls located in various portions of the brain, posessed not only common, but also different antigenic properties.

A clinical-immunologic study of 133 patients was carried out to elucidate the status of the T- and B-immune systems in atherosclerotic dyscirculatory encephalopathy (ADE) in the acute period of cerebral infarction and hemorrhagic stroke. A similar pattern of elevation in humoral and tissue immunity, with quantitative fluctuations in the intensity of individual parameters in various dyscirculatory disorders, was found. The changes indicate that cerebral stroke develops in the body already sensitized in the prestroke period and its development involves the central and peripheric links of the immune system.

Examinations of the clinical and immunological state of 68 patients with the acute stage of cerebral stroke were carried out, and so were immunomorphological examinations of the spleen and the subclavicular lymph nodes in 36 of them whose disease ended in death. An analysis of the results obtained has shown that the immunological reactivity increases from the very first day of the disease. The authors believe that the early immunological response, especially in cases of brain infarction, is due to development of the cerebral stroke in a sensitized body. A rise of selective antibody titres depending on the character of the cerebrovascular disorder was noted: there were: anti-encephalic antibodies targeted at the malacia focus in cases of brain infarction, and antivascular, and to a lesser extent anti-encephalic antibodies in cases of a hemorrhagic stroke. The informative value of the complement fixation test was found to be greater than that of the hemagglutination inhibition test. High degrees of plasmatization of the splenic tissue and the presence of the anti-encephalic immune complexes in it, mainly in cases of brain infarction, also point to the activity of the immunogenesis in the acute stage of the cerebral stroke.