**Table 2.**

*The concentration of the soluble form of the Fas receptor and Fas ligand in the blood serum of patients with T1DM and in persons with a high risk of developing T1DM.*

*The Role of Apoptosis in Autoimmune Destruction of Pancreatic b-Cells DOI: http://dx.doi.org/10.5772/intechopen.108290*

Efficient elimination of autoreactive T lymphocytes from the peripheral blood requires maintaining a balance between cells expressing Fas and FasL. It is important to consider the possible role of the soluble Fas receptor (sFas) in the inhibition of apoptosis via the Fas pathway [30].

Our results on an increase in serum sFas in the state of decompensation of T1DM are consistent with the results of a number of authors who reported an increase in the content of the soluble form of Fas in some systemic and organ-specific autoimmune diseases [31, 37].

The concentration of sFasL in the T1DM compensation group was significantly higher than in the decompensation group and significantly lower than in the risk group (**Table 2**). It should be noted a significant increase in the level of sFasL in the risk group, which is consistent with the literature data [8].

Several experimental studies have shown that both membrane and soluble forms of the Fas ligand (sFasL) are involved in the removal of autoreactive human cells [20, 21]. According to the literature, in an experimental study, preliminary cultivation of diabetogenic T lymphocyte clones with sFasL completely inhibited the development of autoimmune diabetes in mice, which were then transplanted with diabetogenic T cells [20]. This means that the increase in sFasL in T1DM has a protective value and is aimed at establishing peripheral tolerance, which is necessary for protection against autoimmune aggression against b-cells. An increase in sFasL was reported in individuals at high risk of developing T1DM against the background of a decrease in the number of autoreactive CD4+CD95+ and CD8+CD95+-lymphocytes in the blood, in connection with which the authors suggest the involvement of sFasL in the removal of pathogenic T cells at the preclinical stage of the disease [8]. According to the literature, an increase in the soluble form of the Fas ligand (sFasL) is a compensatory mechanism aimed at the elimination of activated autoreactive peripheral blood lymphocytes and plays a protective role.
