**4. Perspectives for the treatment and prevention of T1DM**

It is clear from the above data that the process of apoptosis as the central mechanism of b-cell death in T1DM deserves further study. The field of research into the process of apoptosis is one of the most promising areas in cell biology. In the future, therapeutic intervention could be implemented at the level of immune cells and/or target cells.

The accumulation of knowledge about b-cell apoptosis is likely to progress rapidly in the near future. If apoptosis is the general mechanism by which b-cells die in T1DM in response to immune attacks by cytokines and/or T lymphocytes (cellular cytotoxicity), then new strategies may be developed to prevent the process of b-cell death, and hence the manifestation of the disease itself.

It has been established that protection against apoptosis can be implemented at four different levels: (1) "interception" of stimuli that induce apoptosis; (2) functional antagonism of apoptosis triggers; (3) intervention in the signal cascade; (4) blockade of catabolic enzymes involved in cell self-destruction. The study of all levels of intervention can serve as the basis for the development of a new strategy to prevent the death of b-cells [2, 7].

Treatment aimed at suppressing the initiation of the apoptosis process is promising. For example, some methods may include blockade of death ligand binding (TNF, FasL). In addition, the goals of therapy may be aimed at increasing resistance to apoptotic stimuli by increasing the expression of anti-apoptotic members of the bcl-2 family.
