## 4 Discussion
Intercellular adhesion by ICAM-1 and VCAM-1 is essential for the activation of T-lymphocytes during the process of inflammation. An interaction between ICAM-1 receptor MSCs and the LFA-1 receptor on lymphocytes was observed. It plays an important role in triggering an immune response. MSCs co-cultivated with T lymphocytes in the presence of activation of the T lymphocyte antigen receptor significantly enhance the T lymphocyte adhesion capability by increasing the expression of ICAM-1 and VCAM-1. ICAM-1 and VCAM-1 are inducible in the presence of IFN-\(\gamma\) and tumor necrosis factor alpha (TNF-\(\alpha\)) and IL-1. The immunosuppressive effect of MSCs on T lymphocytes was compared with the change in the intensity of adhesion molecule expression. Higher ICAM-1 expression in activated CMSCs compared to non-activated CMSCs was found. Authors [44] noticed increased expression of ICAM-1 and VCAM-1 after activated splenocytes co-stimulated with activated splenocytes. Adhesive molecules have a significant effect on motility functions. Activated splenocytes were able to enhance the expression of ICAM-1 and VCAM-1. Intercellular contact between lymphocytes and MSCs is required to increase ICAM-1 and VAM-1 levels. It is assumed that increased expression of ICAM-1 and VCAM-1 influences the immunomodulatory ability of MSCs [45]. The stimulation of CMSCs was observed and the presence of IL-10 was also noticed after co-cultivation of CMSCs and lymphocytes. The levels of IL-10 were higher in co-cultivated CMSCs, and the results were statistically significant. The authors [46] observed multiple tissue sources of MSCs. Results show that [PERSON]'s MSCs cause a weak immune response. On the other hand, they have the most powerful immunosuppressive potential compared to MSCs from bone marrow. Recent studies have shown that MSCs respond to danger signals in the environment of inflammation. MSCs express Toll-like receptors in which activation results in significant change and expression of the MSCs and polarization of MSCs on MSC1 or MSC2 phenotypes by TLR4 or TLR3 stimulation. MSC1 has a proinflammatory phenotype and secretion of inflammatory IL-6 and IL-8 interleukins. MSC2 produces anti-inflammatory interleukins [47]. Recent studies have confirmed that the immunomodulatory function of MSCs is coordinated with several types of immune cells. The detailed course of these interactions remains unclear. Several mechanisms of interaction of MSCs and immune cells have been described. In the intercellular contact of MSCs and immune system cells, activation secretion is triggered and in some cases immune cell apoptosis can be induced. It can be said that MSCs are a specific immune cell function coordinator in a particular setting. Immune systems and cells associated with the immune system are linked by processes that result in the production of cytokines and the change in phenotypic traits. Interactions can act to induce inflammatory processes. Many studies report conflicting results in monitoring the production of cytokines and their effects. Not much is known about the function of the cells, which act by immunomodulation. There is some data on the impact of MSCs that are directly active in immunomodulation. MSCs can act suppressively on T lymphocytes, B lymphocytes, antigen-presenting cells (APC) and natural killers (NK). MSCs further act on the differentiation of immune cells and influence the formation of an immunoregulatory phenotype of immune cells with tolerogenic properties. MSCs enter into interactions with regulatory T lymphocytes, regulatory B lymphocytes, regulatory APCs and NK cells, and act together to create a tolerogenic environment that modulates the immune response [48; 49].