Human mesenchymal stem cells (MSCs) are considered to be a promising source of cells in regenerative medicine. They have large potential to differentiate into various tissue-specific populations and may be isolated from diverse tissues in desired quantities. As cells of potential autologous origin, they allow recipients to avoid the alloantigen responses. They also have the ability to create immunomodulatory microenvironment, and thus help to minimize organ damage caused by the inflammation and cells activated by the immune system. Our knowledge about the reparative, regenerative, and immunomodulatory properties of MSCs is advancing. At present, there is a very comprehensible idea on how MSCs affect the immune system, particularly in relation to the tissue and organ damage on immunological basis. Hitherto a number of effective mechanisms have been described by which MSCs influence the immune responses. These mechanisms include a secretion of soluble bioactive agents, an induction of regulatory T cells, modulation of tolerogenic dendritic cells, as well as induction of anergy and apoptosis. MSCs are thus able to influence both innate and adaptive immune responses. Soluble factors that are released into local microenvironment with their subsequent paracrine effects are keys to the activation. As a result, activated MSCs contribute to the restoration of damaged tissues or organs through various mechanisms facilitating reparative and regenerative processes as well as through immunomodulation itself and differentiation into the cells of the target tissue.

Hyaline cartilage, which is characterized by the absence of vascularization and innervation, has minimal self-repair potential in case of damage and defect formation in the chondral layer. Chondrocytes are specialized cells that ensure the synthesis of extracellular matrix components, namely type II collagen and aggregen. On their surface, they express integrins CD44, α1β1, α3β1, α5β1, α10β1, αVβ1, αVβ3, and αVβ5, which are also collagen-binding components of the extracellular matrix. This article aims to contribute to solving the problem of the possible repair of chondral defects through unique methods of tissue engineering, as well as the process of pathological events in articular cartilage. In vitro cell culture models used for hyaline cartilage repair could bring about advanced possibilities. Currently, there are several variants of the combination of natural and synthetic polymers and chondrocytes. In a three-dimensional environment, chondrocytes retain their production capacity. In the case of mesenchymal stromal cells, their favorable ability is to differentiate into a chondrogenic lineage in a three-dimensional culture.

Rheumatoid arthritis (RA) is an autoimmune disease that causes damage to joints. This review focuses on the possibility of influencing the disease through immunomodulation by mesenchymal stem cells (MSCs). There is an occurrence of rheumatoid factor and RA-specific autoantibodies to citrullinated proteins in most patients. Citrulline proteins have been identified in the joints of RA patients, and are considered to be the most suitable candidates for the stimulation of anti-citrulline protein antibodies production. Fibroblast-like proliferating active synoviocytes actively promote inflammation and destruction in the RA joint, in association with pro-inflammatory cells. The inflammatory process may be suppressed by MSCs, which are a population of adherent cells with the following characteristic phenotype: CD105+, CD73+, CD90+, CD45−, CD34− and HLA DR−. Following the stimulation process, MSCs are capable of immunomodulatory action through the release of bioactive molecules, as well as direct contact with the cells of the immune system. Furthermore, MSCs show the ability to suppress natural killer cell activation and dendritic cells maturation, inhibit T cell proliferation and function, and induce T regulatory cell formation. MSCs produce factors that suppress inflammatory processes, such as PGE2, TGF-β, HLA-G5, IDO, and IL-10. These properties suggest that MSCs may affect and suppress the excessive inflammation that occurs in RA. The effect of MSCs on rheumatoid arthritis has been proven to be a suitable alternative treatment thanks to successful experiments and clinical studies.

One of the blends that is usable for 3D printing while not being toxic to cell cultures is the lactic acid (PLA)/polyhydroxybutyrate (PHB)/thermoplastic starch (TPS) blend. The addition of plasticizers can change the rate of biodegradation and the biological behavior of the material. In order to evaluate the potential of the PLA/PHB/TPS material in combination with additives (plasticizers: acetyl tributyl citrate (ATBC) and oligomeric lactic acid (OLA)), for use in the field of biomedical tissue engineering, we performed a comprehensive in vitro characterization of selected mixture materials. Three types of materials were tested: I: PLA/PHB/TPS + 25% OLA, II: PLA/PHB/TPS + 30% ATBC, and III: PLA/PHB/TPS + 30% OLA. The assessment of the biocompatibility of the materials included cytotoxicity tests, such as monitoring the viability, proliferation and morphology of cells and their deposition on the surface of the materials. The cell line 7F2 osteoblasts (Mus musculus) was used in the experiments. Based on the test results, the significant influence of plasticizers on the material was confirmed, with their specific proportions in the mixtures. PLA/PHB/TPS + 25% OLA was evaluated as the optimal material for biocompatibility with 7F2 osteoblasts. The tested biomaterials have the potential for further investigation with a possible change in the proportion of plasticizers, which can have a fundamental impact on their biological properties.

The complex process of placental implantation and development affects trophoblast progenitors and uterine cells through the regulation of transcription factors, cytokines, adhesion receptors and their ligands. Differentiation of trophoblast precursors in the trophectoderm of early ontogenesis, caused by the transcription factors, such as CDX2, TEAD4, Eomes and GATA3, leads to the formation of cytotrophoblast and syncytiotrophoblast populations. The molecular mechanisms involved in placental formation inside the human body along with the specification and differentiation of trophoblast cell lines are, mostly due to the lack of suitable cell models, not sufficiently elucidated. This review is an evaluation of current technologies, which are used to study the behavior of human trophoblasts and other placental cells, as well as their ability to represent physiological conditions both in vivo and in vitro. An in vitro 3D model with a characteristic phenotype is of great benefit for the study of placental physiology. At the same time, it provides great support for future modeling of placental disease.