## 4 Discussion
Monitored cells populations of the CMSCs retained expression of the mesenchymal traits in all seven isolated CMSCs samples between the first and third passage of observation. The preservation MSCs phenotype was confirmed while testing CMSCs immunomodulatory properties. The main purpose of the study was to test the effect of CMSCs on a selected population of immune-active cells. Interactions between cells require intercellular contact and multiple solubility factors. Both cell populations, were monitored in co-cultivation. CMSCs were stimulated with _Poly (I:C)_, similar to viral DNA acting as a TLR3 ligand, in order to activate CMSCs during co-cultivation with activated lymphocytes. A co-cultivation system was used in vitro in order to assess the effect of activated vital fluorescence-labelled CFDA-SE lymphocytes and CMSCs. The intensity of fluorescence in co-cultivation was compared with the pure culture of activated and labelled lymphocytes. Lymphocytes phenotype and CMSCs phenotype were also evaluated after co-cultivation. Results from the following groups were assessed: CMSCs activated _Poly (I:C)_ and CMSCs not activated. In co-cultivation of lymphocytes CMSCs reduced proliferation of activated lymphocytes was observed. The extent of proliferation decline was determined by the fluorescence difference of CFDA-SE labelled lymphocytes over four days of co-cultivation of lymphocytes and CMSCs. In the comparison groups, the co-cultivation of CMSCs and lymphocytes and the second group of isolated lymphocytes, the difference in proliferation of activated lymphocytes was evaluated. The suppression of proliferation of activated lymphocytes stained with CFSE in co-cultivation with CMSCs was observed. The co-cultured lymphocytes fluoresced to a greater extent than the activated self-cultured lymphocytes, which exhibited decreased fluorescence and thus underwent multiple mitoses. In this group, we saw inhibition of activated lymphocytes proliferation. This fact confirmed the immunosuppressive effect of CMSCs indirect contact culture on activated lymphocytes. Suppression proliferation of activated lymphocytes was noticed. Results indicate that CMSCs have immunomodulatory capacity. MSCs respond to the changing environment. In the inflammatory environment, activation of MSCs occurs by occupying specific TLR3 and TLR4 receptors that are associated with the DAMP and PAMP pathogens. This stimulation is alternatively possible via the synthetic analogue of double-stranded (ds) RNA and _Poly (I:C)_. _Poly (I:C)_ was used to stimulate CMSCs. Afterwards, the expression of surface and adhesion markers was tested. MSCs have enhanced expression of ICAM-1, the vascular cell adhesion molecule 1 (VCAM-1), and chemokine ligand 3 (CXCR3) ligands that are CXCR3-activated T lymphocyte ligands under inflammatory conditions. Many processes in the immune environment are caused by interactions of adhesion molecules. The molecules mediate the accumulation of immune cells and allow their close contact with MSCs. MSCs come into contact with T cells in the inflammatory environment. It is assumed that ICAM-1 and VCAM-1 have a significant effect on the MSCs-mediated immunomododulation. The expression of the adhesion molecules MSCs increases with inflammatory cytokines. Interactions between VCAM-1 and endothelial integrins have been demonstrated. VCAM-1 is a late-activating antigen ligand 4 (VLA-4) and ICAM-1 is a ligand for LFA-1. Recent studies have shown that after stimulation, MSCs produce inflammatory cytokines that are attractants for lymphocytes. The ICAM-1 and VCAM-1 molecules are considered to be co-stimulatory in the immune response. ICAM-1 and VCAM-1 play an important role in MSCs-mediated immunosuppression, thanks to their ability to interact with lymphocytes and MSCs. These adhesion molecules play a crucial role in specific immune responses to foreign pathogens. Adhesive molecules interact with lymphocytes and endothelium. Upon reaching the endothelium, adhesion molecules mediate cell movement [43].