The human body responds to oxidative stress, a driver of sterile inflammation, by using the mechanisms of innate immunity, through the recognition of damage-associated molecular patterns (DAMP). During oxidative stress cells remove oxidized molecules by releasing stress derived extracellular vesicles (sEV). sEVs mediate intercellular communication. In this way they can also drive adaptive immune response in the direction of various T lymphocytes effector cells. The latter depends mainly on the account of consistent activation and maturation of dendritic cells. In the scope of the master's thesis, we therefore wanted to evaluate the influence of sEV on the differentiation of T lymphocytes, especially via the IL-23/Th17 pathway. Although endogenous ligands act through the same receptors as ligands in microbes, they elicited a different immune response, as shown by differences in LPS signaling versus sEV. After stimulation of dendritic cells with sEV by using qPCR we determined mRNA expression of proinflammatory cytokines, primarily Il23, as well as other cytokines. Naive T CD4 + lymphocytes isolated from the spleen were stimulated by dendritic cell culture, and the concentration of cytokines IL-17 in IL-2 was monitored by ELISA. The results of the study showed that the amount of cytokines secreted from dendritic cells was not sufficient for successful differentiation of T lymphocytes into Th17 type or Th1 type. Repeated stimulation with sEV and longer cultivation time in co-culture slightly increased the secretion of IL-17, but was not enough to show a successful differentiation of Th17 cells. The exact molecular mechanism of action of sEV on T lymphocyte differentiation still remains partially unknown. In the future, additional research will be needed to clarify this mechanism, especially in terms of its activation, the consequences of activation in relation to chronic diseases, and ways to inhibit it.