**10. T1D and vaccination: Is there a correlation between them? The role of passive immunization in T1D development**

There exist quite a few hypotheses concerning the role of vaccination in triggering autoimmune diseases including T1D. This fact notwithstanding, only few instances proved to display a clearcut correlation between vaccination and development of autoimmune syndromes. (Ethan Rubinstein, 2004) In the meantime, heated discussions about association between autoimmune disorders and vaccination do not abate. Advocates of the "autoimmunization" hypothesis refer to recent flagrant global-scale spreading of autoimmune diseases with a particular on responsibility of children's vaccines manufacturers. (Classen JB & Classen DC, 1999)

There is evidence that T1D indeed develop in response to immunization. At the same time, in newborn infants vaccinated at the age of several months the incidence of T1D did not exceed the morbidity level in children immunized with a single vaccinating dose at the age of 2 years. (Karvonen et al., 1999) Mass-scale serial investigations carried out in the USA did not establish any associativity between these two events. Similarly, studies into the role of vaccination and vaccination timing as risk factors in childhood diabetes failed to establish a correlation between vaccination and the risk for autoimmune diseases. (DeStefano et al., 2001; Blom et al., 2001)

Preclinical and Predictive Algorithms in Monitoring

**12.1 State-of-art models of multiple sclerosis**

(Sepiashvili et al., 2010; Martynov et al., 2010)

**13. Aortic aneurisms** 

curative treatment.

degeneration of axons.

**12. Multiple Sclerosis (MS)** 

Patients with Autoimmune Diseases and Their Relatives-at-Risks 213

dynamic control over disease progression, but also enables the physician to estimate the efficiency of ongoing therapy, to search for early-stage biomarkers for diagnosing secondary autoimmune disorders and, last but not least, to implement adequate preventive and

Multiple sclerosis (MS), a remitting and relapsing autoimmune disease of the central nervous system (CNS), represents a generalized degenerative inflammatory process. Its main causative factors are demyelination, degradation of oligodendrocytes and

The clinical course of MS includes three stages, viz., the preclinical stage, the autoimmune inflammation stage and the neurodegeneration stage. Some basically important targets (including gene-oriented ones) emerging in the course of MS evolution can be used in the design of novel preclinical diagnostic tools. Expression of gene products including functionally important transcripts is currently employed in the design of proteomes. The use of these constructs (commonly referred to as diagnostic microchips) as early as at the preclinical pathology stage allows multifarious manipulations with specific targets in the course of immune attacks. Impaired structure of the myelin sheath (demyelination) and degradation of axons take place at the very earliest stages of preclinical MS, i.e., long before the clinical onset of the disease. This generates a need for innovative preclinical diagnosis protocols and, in a more distant perspective, preventive treatment of MS. In this context, genetic tests acquire special importance as valuable analytical tools for predicting and estimating risks in MS. In terms of present-day classifications, the genes supporting predisposition to MS are divided into three main groups, viz., immune system genes (DRB1, OPN, CD44, CD24, CCR5-Δ32), myelin metabolism genes (MBP, CTLA4, ICAM1) and cytokins (TGFβ1, TNF). AutoAbs to the basic protein of myelin are amont the key autoaggression markers for demyelination-related pathologies. Some of these Abs have functional resources of their own, e.g., proteolytic activity towards the Ag substrate. The dynamics of Abs spectra in patients with MS reflect etiogenic peculiarities of MS evolution. It is now well established that pre-early stages of MS are accompanied by the appearance of specific Abs against two categories of determinants, viz., mimicking and myelin epitopes. After termination of the preclinical phase, serum titers of mimicking Abs show a tendency to decrease, while those of antimyelin and antineural autoAbs increase in contrast. This upward trend points to escalation of antitissue autoaggression and formation of a typical clinical picture of the disease including a complete set of clinical and serological criterial features of PIFAS. Early emergence and long persistence of antimyelin autoAbs in MS patients points to a correlation between serum positivity and duration of the disease.

Aortic aneurisms (AA) are related to the category of socially important diseases involving a high risk for lethality. Its main causal factors are degradation of elastin (e.g., by proteases), pronounced structural changes in medial smooth muscle cells (SMC), aortic vasculature atrophies and formation of the *preclinical* pathological syndrome. The main clinically
