Molecular mimicry between human and microbial/viral/parasite peptides is common and has long been associated with the etiology of autoimmune disorders provoked by exogenous pathogens. A growing body of evidence accumulated in recent years suggests a strong correlation between SARS-CoV-2 infection and autoimmunity. The article analyzes the immunogenic potential of the peptides shared between the SARS-CoV-2 spike glycoprotein (S-protein) and antigens of human endocrinocytes involved in most common autoimmune endocrinopathies. A total of 14 pentapeptides shared by the SARS-CoV-2 S-protein, thyroid, pituitary, adrenal cortex autoantigens and beta-cells of the islets of Langerhans were identified, all of them belong to the immunoreactive epitopes of SARS-CoV-2. The discussion of the findings relates the results to the clinical correlates of COVID-19-associated autoimmune endocrinopathies. The most common of these illnesses is an autoimmune thyroid disease, so the majority of shared pentapeptides belong to the marker autoantigens of this disease. The most important in pathogenesis of severe COVID-19, according to the authors, may be autoimmunity against adrenals because their adequate response prevents excessive systemic action of the inflammatory mediators causing cytokine storm and hemodynamic shock. A critique of the antigenic mimicry concept is given with an assertion that peptide sharing is not a guarantee but only a prerequisite for provoking autoimmunity based on the molecular mimicry. The latter event occurs in carriers of certain HLA haplotypes and when a shared peptide is only used in antigen processing

Anti-idiotypic antibodies (anti-IDs) were discovered at the very beginning of the 20th century and have attracted attention of researchers for many years. Nowadays, there are five known types of anti-IDs: α, β, γ, ε, and δ. Due to the ability of internal-image anti-IDs to compete with an antigen for binding to antibody and to alter the biologic activity of an antigen, anti-IDs have become a target in the search for new treatments of autoimmune illnesses, cancer, and some other diseases. In this review, we summarize the data about anti-IDs that mimic the structural and functional properties of some bioregulators (autacoids, neurotransmitters, hormones, xenobiotics, and drugs) and evaluate their possible medical applications. The immune system is potentially able to reproduce or at least alter the effects of any biologically active endogenous or exogenous immunogenic agent via the anti-idiotypic principle, and probably regulates a broad spectrum of cell functions in the body, being a kind of universal remedy or immunacea, by analogy to the legendary ancient goddess of universal healing Panacea (Πανάκεια, Panakeia in Greek) in the treatment and prevention of diseases, possibly including non-infectious somatic and even hereditary ones.

The compound 4-thioureidoiminomethylpyridinium perchlorate (perchlozone^©) is a novel anti-tuberculosis drug that is active in multiple drug resistance cases, but the compound is hepatotoxic. To decrease the systemic load and to achieve targeting, we encapsulated the drug into poly(lactic acid)-based micro- (1100 nm) and nanoparticles (170 nm) that were modified with single-chain camel immunoglobulin G (IgG) for targeting. Both micro- and nanoparticles formed stable suspensions in saline solution at particle concentrations of 10–50 mg/mL. The formulations were injected intraperitoneally and intravenously into the mice with experimental tuberculosis. The survival of control animals was compared to that of mice which were treated with daily oral drug solution, single intraperitoneal administration of drug-loaded particles, and those treated both intravenously and intraperitoneally by drug-loaded particles modified with polyclonal camel IgGs. The distribution of particles in the organs of mice was analyzed with immunofluorescence and liquid chromatography/mass spectrometry. Morphological changes related to tuberculosis and drug toxicity were registered. Phagocytic macrophages internalized particles and transported them to the foci of tuberculosis in inner organs. Nanoparticle-based drug formulations, especially those with IgG, resulted in better survival and lower degree of lung manifestations than the other modes of treatment.

In order to identify corresponding amino acid sequences (pentapeptides) between the SPs, MPs and NPs of human coronaviruses and human autoantigens targeted in autoimmune endocrinopathies, and for a comparative analysis of the various coronaviruses proteome and the proteome of human, the original computer program was used. Quantitatively, SP, MP and NP of the human coronaviruses were found to share totally 117 minimal immune pentapeptide epitopes: 79 in SP, 14 in MP and 24 in NP, – with 18 autoantigens expressed by human endocrinocytes. The shared pentapeptides belong to the proteins of human endocrine cells. Samples of the pituitary, adrenal and thyroid from patients who died from coronavirus infection (COVID-19) were studied morphologically using histochemical methods. A high incidence of SARS-CoV-2 infection of endocrine cells was showed. The high affinity of SARS-CoV-2 the cells of the adenohypophysis was revealed, but there was no expression of viral proteins by the cells of the neurohypophysis. The foci of lesions in endocrine organs contained abundant lymphocytic infiltrates which may indicate the impact of autoimmune processes. Autoimmune disorders have a multi-faceted etiology and depend on polygenic predispose and additive action of many epigenetic and environmental factors causing hyperstimulation of imperfectly functioning immune system. It means that the phenomenon of molecular mimicry cannot be blamed as their single prerequisite, but it is just a tile in mosaic of autoimmunity. The facts revealed emphasize the need of endocrinological diagnostic alertness of a physician while observing patients with post-vaccination and post-COVID-19 health disorders.

The review presents data on two similar granulomatous inflammatory diseases: tuberculosis and sarcoidosis of the lungs, which together cover about 5% of all pulmonary pathology, albeit occur with different incidence (20 : 1). Despite the established aetiology of tuberculosis, the disease has not disappeared and nowadays has even acquired a new urgency: It is getting out of control due to growing poverty, the comorbidity with HIV infection, increasing cases of drug resistance of Mycobacteria, insufficient effectiveness and the growing costs of its treatment. Against the background of the expansion of anthropogenic influences and other environmental impacts on the immune system, the incidence of lung sarcoidosis is also increasing, while patients are initially often misdiagnosed with tuberculosis, with resulting unjustified anti-tuberculosis chemotherapy, leading to chronization of the disease with frequent relapses and, accordingly, to an increase in disability and mortality rates. In recent years, clinical manifestations of sarcoidosis due to a variety of trigger aetiological factors with adjuvant-like action (from Mycobacteria to xenobiotics) are considered by a number of authors as a variant of autoimmune/autoinflammatory syndrome induced by adjuvants (ASIA). The article emphasizes the similarity of two granulomatous inflammatory diseases and the concept of two variants of the bodys response to similar or even identical aetiological factors within different human reactivity (possibly on a different mosaic/permissive background). In brief the newest data on experimental models of sarcoidosis are reviewed as well as the role of autophagy disorders and opposite macrophageal polarization in tuberculosis versus sarcoidosis. Authors coined the original hypothesis of the possible therapeutic effectiveness of Rapamycin in sarcoidosis and for the first time posed a question of equivocal character of comorbidity between these granulomatoses and COVID-19 infection.

Today, autoimmune Hashimoto´s thyroiditis is the most common cause of hypothyroidism. Thyroid hormones are involved in almost all metabolic processes, their deficiency leads to disruption of metabolic processes in all organs and systems, which is the reason for the rich clinical picture and variety of symptoms of hypothyroidism. The deficiency of thyroid hormones also has a significant negative impact on a person's mental health, identifying a diverse clinical picture – from mild disorders to serious mental disorders. For hypothyroidism, such psycho-neurological changes as drowsiness, weakness, loss of interest in the surroundings, loss of memory and intelligence are also characteristic. Delirious and delirious-hallucinatory conditions are described, as well as anxious and depressive conditions. Hypothyroid psychoneurological disorders have recently become more common, and therefore their diagnosis and correction are becoming more urgent. Persons with hypothyroi dism often mistakenly go not to the endocrinologist, but to a psychiatrist and receive therapy, but psychotropic drugs and antidepressants in hypothyroidism don´t give the proper effect and even are contraindicated. Hypocalcemia is very often observed with Hashimoto´s thyroiditis, it can be explained by autoimmune parathyroiditis with a hypoparathyroid clinic, that is, with autoimmune thyroiditis, the function of parathyroid glands may be disrupted. The article presents the results of our own research. A group of patients with autoimmune thyroiditis and hypothyroidism was examined. Complaints, anamnesis and clinic of the disease, levels of TSH, thyroid hormones, total and ionized calcium, inorganic phosphorus, vitamin D3 were studied.