@article{MTMT:35316198,
	title = {Role of the GalNAc-galectin pathway in the healing of premature rupture of membranes},
	url = {https://m2.mtmt.hu/api/publication/35316198},
	author = {Chen, Jia-Le and Liu, Lou and Peng, Xin-Rui and Wang, Yan and Xiang, Xiang and Chen, Yu and Xu, De-Xiang and Chen, Dao-Zhen},
	doi = {10.1186/s10020-024-00908-6},
	journal-iso = {MOL MED},
	journal = {MOLECULAR MEDICINE},
	volume = {30},
	unique-id = {35316198},
	issn = {1076-1551},
	keywords = {galectin; healing; PROM; N-acetyl-D-galactosamine},
	year = {2024},
	eissn = {1528-3658}
}

@article{MTMT:35657394,
	title = {Cell-based and extracellular vesicle-based MSC therapies for acute radiation syndrome affecting organ systems},
	url = {https://m2.mtmt.hu/api/publication/35657394},
	author = {Miura, Y. and Fujii, S. and Ichinohe, T.},
	doi = {10.1093/jrr/rrae009},
	journal-iso = {J RADIAT RES},
	journal = {JOURNAL OF RADIATION RESEARCH},
	volume = {65},
	unique-id = {35657394},
	issn = {0449-3060},
	year = {2024},
	eissn = {1349-9157},
	pages = {i80-i87}
}

@article{MTMT:35133023,
	title = {Characterization of obesity-related diseases and inflammation using single cell immunophenotyping in two different diet-induced obesity models},
	url = {https://m2.mtmt.hu/api/publication/35133023},
	author = {Ruppert, Zsófia and Neuperger, Patricia and Rákóczi, Bettina and Gémes, Nikolett and Dukay, Brigitta and Hajdu, Petra and Péter, Mária and Balogh, Gábor and Tiszlavicz, László and Vigh, László and Török, Zsolt and Puskás, László and Szebeni, Gábor and Tóth, Erzsébet Melinda},
	doi = {10.1038/s41366-024-01584-6},
	journal-iso = {INT J OBES (LOND)},
	journal = {INTERNATIONAL JOURNAL OF OBESITY},
	volume = {48},
	unique-id = {35133023},
	issn = {0307-0565},
	abstract = {Obesity is a growing problem worldwide and a major risk factor for many chronic diseases. The accumulation of adipose tissue leads to the release of significant amounts of pro-inflammatory cytokines and adipokines, resulting in a low-grade systemic inflammation. However, the mechanisms behind the development of obesity-related diseases are not fully understood. Therefore, our study aimed to investigate the pathological changes and inflammatory processes at systemic level and in individual organs in two different diet-induced mouse obesity models.},
	year = {2024},
	eissn = {1476-5497},
	pages = {1568-1576},
	orcid-numbers = {Tiszlavicz, László/0000-0003-1134-6587; Szebeni, Gábor/0000-0002-6998-5632}
}

@article{MTMT:34566506,
	title = {Mesenchymal stromal cells in myeloid malignancies: Immunotherapeutic opportunities},
	url = {https://m2.mtmt.hu/api/publication/34566506},
	author = {Vukotić, M. and Kapor, S. and Simon, F. and Cokic, V. and Santibanez, J.F.},
	doi = {10.1016/j.heliyon.2024.e25081},
	journal-iso = {HELIYON},
	journal = {HELIYON},
	volume = {10},
	unique-id = {34566506},
	abstract = {Myeloid malignancies are clonal disorders of the progenitor cells or hematopoietic stem cells, including acute myeloid leukemia, myelodysplastic syndromes, myeloproliferative malignancies, and chronic myelomonocytic leukemia. Myeloid neoplastic cells affect the proliferation and differentiation of other hematopoietic lineages in the bone marrow and peripheral blood, leading to severe and life-threatening complications. Mesenchymal stromal cells (MSCs) residing in the bone marrow exert immunosuppressive functions by suppressing innate and adaptive immune systems, thus creating a supportive and tolerant microenvironment for myeloid malignancy progression. This review summarizes the significant features of MSCs in myeloid malignancies, including their role in regulating cell growth, cell death, and antineoplastic resistance, in addition to their immunosuppressive contributions. Understanding the implications of MSCs in myeloid malignancies could pave the path for potential use in immunotherapy. © 2024 The Authors},
	keywords = {Cell Differentiation; MYELOID CELLS; mesenchymal stromal cells; Myeloid malignancies; T-cell immunosuppression therapy},
	year = {2024},
	eissn = {2405-8440}
}

@article{MTMT:34093747,
	title = {Galectin-1 as a marker for microglia activation in the aging brain},
	url = {https://m2.mtmt.hu/api/publication/34093747},
	author = {Kiss, Tamás and Mir, Mohd Yaqub and Stefancsik, Gergely and Ganbat, Gantulga and Askarova, Aruzhan and Monostori, Éva and Dulka, Karolina and Szebeni, Gábor and Nyúl-Tóth, Ádám and Csiszar, Anna and Légrádi, Ádám},
	doi = {10.1016/j.brainres.2023.148517},
	journal-iso = {BRAIN RES},
	journal = {BRAIN RESEARCH},
	volume = {1818},
	unique-id = {34093747},
	issn = {0006-8993},
	abstract = {Microglia cells, the immune cells residing in the brain, express immune regulatory molecules that have a central role in the manifestation of age-related brain characteristics. Our hypothesis suggests that galectin-1, an anti-inflammatory member of the beta-galactoside-binding lectin family, regulates microglia and neuroinflammation in the aging brain. Through our in-silico analysis, we discovered a subcluster of microglia in the aged mouse brain that exhibited increased expression of galectin-1 mRNA. In our Western blotting experiments, we observed a decrease in galectin-1 protein content in our rat primary cortical cultures over time. Additionally, we found that the presence of lipopolysaccharide, an immune activator, significantly increased the expression of galectin-1 protein in microglial cells. Utilizing flow cytometry, we determined that a portion of the galectin-1 protein was localized on the surface of the microglial cells. As cultivation time increased, we observed a decrease in the expression of activation-coupled molecules in microglial cells, indicating cellular exhaustion. In our mixed rat primary cortical cell cultures, we noted a transition of amoeboid microglial cells labeled with OX42(CD11b/c) to a ramified, branched phenotype during extended cultivation, accompanied by a complete disappearance of galectin-1 expression. By analyzing the transcriptome of a distinct microglial subpopulation in an animal model of aging, we established a correlation between chronological aging and galectin-1 expression. Furthermore, our in vitro study demonstrated that galectin-1 expression is associated with the functional activation state of microglial cells exhibiting specific amoeboid morphological characteristics. Based on our findings, we identify galectin-1 as a marker for microglia activation in the context of aging.},
	keywords = {Aging; Galectin-1; neuroinflammation; microglia},
	year = {2023},
	eissn = {1872-6240},
	orcid-numbers = {Kiss, Tamás/0000-0001-5339-5227; Stefancsik, Gergely/0000-0002-2098-652X; Monostori, Éva/0000-0002-7442-3562; Dulka, Karolina/0000-0002-7368-8198; Szebeni, Gábor/0000-0002-6998-5632; Légrádi, Ádám/0000-0001-7994-1935}
}

@article{MTMT:33081050,
	title = {Immunomodulatory and Regenerative Effects of MSC-Derived Extracellular Vesicles to Treat Acute GVHD},
	url = {https://m2.mtmt.hu/api/publication/33081050},
	author = {Fujii, Sumie and Miura, Yasuo},
	doi = {10.1093/stmcls/sxac057},
	journal-iso = {STEM CELLS},
	journal = {STEM CELLS},
	volume = {40},
	unique-id = {33081050},
	issn = {1066-5099},
	abstract = {The development of human mesenchymal stromal/stem cell (MSC)-based therapy has focused on exploring biological nanoparticles secreted from MSCs. There is emerging evidence that the immunomodulatory and regenerative effects of MSCs can be recapitulated by extracellular vesicles released from MSCs (MSC-EVs). Off-the-shelf allogeneic human MSC products are clinically available to treat acute graft-versus-host disease (GVHD), but real-world data have revealed the limitations of these products as well as their feasibility, safety, and efficacy. MSC-EVs may have advantages over parental MSCs as drugs because of their distinguished biodistribution and importantly dose-dependent therapeutic effects. Recent research has shed light on the role of microRNAs in the mode-of-action of MSC-EVs. A group of specific microRNAs alone or in combination with membrane proteins, membrane lipids, and soluble factors present in MSC-EVs play key roles in the regulation of GVHD. In this concise review, we review the regulation of T-cell-mediated adaptive immunity and antigen-presenting cell-mediated innate immunity by MSC-EVs and the direct regenerative effects on damaged cells in association with the immunopathology of GVHD.},
	keywords = {INJURY; DENDRITIC CELLS; regeneration; Stromal Cells; Oncology; MOUSE MODEL; microRNA; CELL BIOLOGY; GVHD; Mesenchymal Stem Cells; MESENCHYMAL STEM-CELLS; MICROVESICLES; VERSUS-HOST-DISEASE; Exosomes; Extracellular vesicles; M2 macrophages; Biotechnology & Applied Microbiology; circular RNA; Cell & Tissue Engineering; EXOSOMES CONTRIBUTE},
	year = {2022},
	eissn = {1549-4918},
	pages = {977-990},
	orcid-numbers = {Miura, Yasuo/0000-0001-9654-1300}
}

@article{MTMT:32888529,
	title = {Galectin 1-A Key Player between Tissue Repair and Fibrosis},
	url = {https://m2.mtmt.hu/api/publication/32888529},
	author = {Hermenean, Anca and Oatis, Daniela and Herman, Hildegard and Ciceu, Alina and D'Amico, Giovanbattista and Trotta, Maria Consiglia},
	doi = {10.3390/ijms23105548},
	journal-iso = {INT J MOL SCI},
	journal = {INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES},
	volume = {23},
	unique-id = {32888529},
	issn = {1661-6596},
	abstract = {Galectins are ten family members of carbohydrate-binding proteins with a high affinity for beta galactose-containing oligosaccharides. Galectin-1 (Gal-1) is the first protein discovered in the family, expressed in many sites under normal and pathological conditions. In the first part of the review article, we described recent advances in the Gal-1 modulatory role on wound healing, by focusing on the different phases triggered by Gal-1, such as inflammation, proliferation, tissue repair and re-epithelialization. On the contrary, Gal-1 persistent over-expression enhances angiogenesis and extracellular matrix (ECM) production via PI3K/Akt pathway activation and leads to keloid tissue. Therefore, the targeted Gal-1 modulation should be considered a method of choice to treat wound healing and avoid keloid formation. In the second part of the review article, we discuss studies clarifying the role of Gal-1 in the pathogenesis of proliferative diabetic retinopathy, liver, renal, pancreatic and pulmonary fibrosis. This evidence suggests that Gal-1 may become a biomarker for the diagnosis and prognosis of tissue fibrosis and a promising molecular target for the development of new and original therapeutic tools to treat fibrosis in different chronic diseases.},
	keywords = {EXPRESSION; IN-VIVO; PROTEIN; MOLECULAR-MECHANISMS; Wound healing; diabetic retinopathy; diabetic nephropathy; galectin 1; Fibrosis; HYPOXIA; ENDOTHELIAL GROWTH-FACTOR; liver fibrosis; HEPATIC STELLATE CELLS; Biochemistry & Molecular Biology; pancreatic fibrosis; PROLIFERATIVE DIABETIC-RETINOPATHY; CUTANEOUS SCARRING PATHOPHYSIOLOGY},
	year = {2022},
	eissn = {1422-0067},
	orcid-numbers = {Hermenean, Anca/0000-0001-8510-6653; Herman, Hildegard/0000-0002-6741-0245; Ciceu, Alina/0000-0001-6502-2655; Trotta, Maria Consiglia/0000-0001-9813-5955}
}

@article{MTMT:33586986,
	title = {Tumor necrosis factor-alpha-primed mesenchymal stem cell-derived exosomes promote M2 macrophage polarization via Galectin-1 and modify intrauterine adhesion on a novel murine model},
	url = {https://m2.mtmt.hu/api/publication/33586986},
	author = {Li, Jingman and Pan, Yuchen and Yang, Jingjing and Wang, Jiali and Jiang, Qi and Dou, Huan and Hou, Yayi},
	doi = {10.3389/fimmu.2022.945234},
	journal-iso = {FRONT IMMUNOL},
	journal = {FRONTIERS IN IMMUNOLOGY},
	volume = {13},
	unique-id = {33586986},
	issn = {1664-3224},
	abstract = {BackgroundIntrauterine adhesion (IUA) is a condition caused due to damage or infection of the endometrium. It is characterized by continuous inflammation and following fibrosis and dysfunction. However, the current animal IUA models have several disadvantages, including complex operation, high mortality, and many extra distractions owing to opening of the abdominal cavity to expose the uterus. Mesenchymal stem cells (MSCs), which have been used in treatment of IUA, are heterogeneous and immunosuppressive. However, their therapeutic effect is not as good as expected. MethodsHere, we successfully built a new murine IUA model, called electric tool-scratching IUA model, and applied it in our experiments to investigate the efficacy of tumor necrosis factor-alpha (TNF-alpha) primed MSCs (T-MSCs). In the new model, we used a self-made electric tool that can cause mechanical damage to the endometrium without opening the abdominal cavity. ELISA and histological staining analysis were performed to evaluate pathological features of IUA. qRT-PCR, flow cytometry and immunofluoresence staining were performed to detect the phenotypes of macrophages. TMT proteomics quantification and western blotting assay were performed to analyze the differentially expressed proteins of MSC exosomes. ResultsBased on the new IUA model, we found TNF-alpha pretreatment could enhance the ability of MSCs to relieve inflammation and reduce endometrium fibrosis. Mechanistically, T-MSC promoted macrophage polarization to M2 phenotype through exosomes. Subsequently, we found the expression of Galectin-1 was increased in T-MSC exosomes. Finally, we analyzed the gene expression pattern of Galectin-1 treated macrophages and found Galectin-1 promoted macrophage polarization to M2 phenotype mainly through the Jak-STAT signaling pathway. ConclusionsOur studies proposed an innovative mouse model and a better MSC treatment strategy for IUA.},
	keywords = {EXPRESSION; MACROPHAGES; PROLIFERATION; TRANSPLANTATION; EFFICACY; SCAFFOLD; Mesenchymal Stem Cells; Exosomes; Intrauterine adhesions},
	year = {2022},
	eissn = {1664-3224}
}

@article{MTMT:33066488,
	title = {Cellular and Molecular Mechanism of Pulmonary Fibrosis Post-COVID-19: Focus on Galectin-1,-3,-8,-9},
	url = {https://m2.mtmt.hu/api/publication/33066488},
	author = {Oatis, Daniela and Simon-Repolski, Erika and Balta, Cornel and Mihu, Alin and Pieretti, Gorizio and Alfano, Roberto and Peluso, Luisa and Trotta, Maria Consiglia and D'Amico, Michele and Hermenean, Anca},
	doi = {10.3390/ijms23158210},
	journal-iso = {INT J MOL SCI},
	journal = {INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES},
	volume = {23},
	unique-id = {33066488},
	issn = {1661-6596},
	abstract = {Pulmonary fibrosis is a consequence of the pathological accumulation of extracellular matrix (ECM), which finally leads to lung scarring. Although the pulmonary fibrogenesis is almost known, the last two years of the COVID-19 pandemic caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and its post effects added new particularities which need to be explored. Many questions remain about how pulmonary fibrotic changes occur within the lungs of COVID-19 patients, and whether the changes will persist long term or are capable of resolving. This review brings together existing knowledge on both COVID-19 and pulmonary fibrosis, starting with the main key players in promoting pulmonary fibrosis, such as alveolar and endothelial cells, fibroblasts, lipofibroblasts, and macrophages. Further, we provide an overview of the main molecular mechanisms driving the fibrotic process in connection with Galactin-1, -3, -8, and -9, together with the currently approved and newly proposed clinical therapeutic solutions given for the treatment of fibrosis, based on their inhibition. The work underlines the particular pathways and processes that may be implicated in pulmonary fibrosis pathogenesis post-SARS-CoV-2 viral infection. The recent data suggest that galectin-1, -3, -8, and -9 could become valuable biomarkers for the diagnosis and prognosis of lung fibrosis post-COVID-19 and promising molecular targets for the development of new and original therapeutic tools to treat the disease.},
	keywords = {Inflammation; EXPRESSION; CELLS; SONIC HEDGEHOG; galectin; binding protein; lung fibrosis; MESENCHYMAL TRANSITION; Galectin-3; Pulmonary Fibrosis; Biochemistry & Molecular Biology; TISSUE GROWTH-FACTOR; COVID-19},
	year = {2022},
	eissn = {1422-0067},
	orcid-numbers = {Balta, Cornel/0000-0001-5734-0071}
}

@article{MTMT:32182436,
	title = {Galectin-1 secreted by bone marrow-derived mesenchymal stem cells mediates anti-inflammatory responses in acute airway disease},
	url = {https://m2.mtmt.hu/api/publication/32182436},
	author = {Ge, X. and Shi, K. and Hou, J. and Fu, Y. and Xiao, H. and Chi, F. and Xu, J. and Cai, F. and Bai, C.},
	doi = {10.1016/j.yexcr.2021.112788},
	journal-iso = {EXP CELL RES},
	journal = {EXPERIMENTAL CELL RESEARCH},
	volume = {407},
	unique-id = {32182436},
	issn = {0014-4827},
	abstract = {The hallmarks of allergic airway disease (AAD) include infiltration of inflammatory cells into the bronchoalveolar space. Bone marrow derived mesenchymal stem cells (BMSCs) show anti-inflammatory properties in AAD. In addition, galectin-1 (Gal-1) is a lectin significantly upregulated upon inflammation and is also known to mediate potential anti-inflammatory responses. We hypothesized that BMSCs regulated inflammatory responses by secretion of Gal-1 during AAD pathogenesis. BMSCs were isolated from murine femurs and tibiae and adoptively transferred into an ovalbumin-induced AAD mouse model. Knockdown of Gal-1 in BMSCs was performed using shRNA. Flow cytometry, ELISAs, and immunohistology were performed to analyze inflammatory responses in mice, and a Transwell system was used to establish an in vitro co-culture system of lung epithelial cells (MLE-12) and BMSCs. Administration of BMSCs significantly upregulated Gal-1 expression upon inflammation and decreased infiltration of inflammatory cells and secretion of proinflammatory cytokines in vivo. In addition, we showed that this function was mediated by reduced activation of the MAPK p38 signaling pathway. Similar observations were found using an in vitro lipopolysaccharide-induced model when MLE-12 cells were co-cultured with BMSCs. Gal-1 secretion by BMSCs alleviated inflammatory responses observed in AAD and hence provides a promising therapeutic alternative to AAD patients insensitive to conventional drug treatments. © 2021 Elsevier Inc.},
	keywords = {Galectin-1; anti-inflammatory; Mesenchymal Stem Cells; Acute airway disease},
	year = {2021},
	eissn = {1090-2422}
}

@article{MTMT:32106566,
	title = {Myeloid-Derived Suppressor Cells and Mesenchymal Stem/Stromal Cells in Myeloid Malignancies},
	url = {https://m2.mtmt.hu/api/publication/32106566},
	author = {Kapor, Suncica and Santibanez, Juan F.},
	doi = {10.3390/jcm10132788},
	journal-iso = {J CLIN MED},
	journal = {JOURNAL OF CLINICAL MEDICINE},
	volume = {10},
	unique-id = {32106566},
	abstract = {Myeloid malignancies arise from an altered hematopoietic stem cell and mainly comprise acute myeloid leukemia, myelodysplastic syndromes, myeloproliferative malignancies, and chronic myelomonocytic leukemia. Myeloid neoplastic leukemic cells may influence the growth and differentiation of other hematopoietic cell lineages in peripheral blood and bone marrow. Myeloid-derived suppressor cells (MDSCs) and mesenchymal stromal cells (MSCs) display immunoregulatory properties by controlling the innate and adaptive immune systems that may induce a tolerant and supportive microenvironment for neoplasm development. This review analyzes the main features of MDSCs and MSCs in myeloid malignancies. The number of MDSCs is elevated in myeloid malignancies exhibiting high immunosuppressive capacities, whereas MSCs, in addition to their immunosuppression contribution, regulate myeloid leukemia cell proliferation, apoptosis, and chemotherapy resistance. Moreover, MSCs may promote MDSC expansion, which may mutually contribute to the creation of an immuno-tolerant neoplasm microenvironment. Understanding the implication of MDSCs and MSCs in myeloid malignancies may favor their potential use in immunotherapeutic strategies.},
	keywords = {BONE-MARROW; GROWTH-FACTOR-BETA; T-CELLS; Up-Regulation; Stromal Cells; neoplasm; Myelodysplastic Syndromes; Chronic myelogenous leukemia; MARROW STROMAL CELLS; HEMATOPOIETIC STEM-CELL; Myeloid-derived suppressor cells; Mesenchymal stem; chimeric antigen receptors; Myeloid malignancies; T-cell immunosuppression},
	year = {2021},
	eissn = {2077-0383}
}

@article{MTMT:32073571,
	title = {APPLICATION OF MULTIPOTENT MESENCHYMAL STEM CELL SECRETOME IN THE TREATMENT OF ADJUVANT ARTHRITIS AND CONTACT-ALLERGIC DERMATITIS IN ANIMAL MODELS},
	url = {https://m2.mtmt.hu/api/publication/32073571},
	author = {Golubinskaya, P. A. and Sarycheva, M. V and Dolzhikov, A. A. and Bondarev, V. P. and Stefanova, M. S. and Soldatov, V. O. and Nadezhdin, S. V and Korokin, M. V and Pokrovsky, M. V and Burda, Yu E.},
	doi = {10.19163/2307-9266-2020-8-6-416-425},
	journal-iso = {PHARM PHARMACOL-RUSS},
	journal = {PHARMACY & PHARMACOLOGY-FARMATSIYA I FARMAKOLOGIYA},
	volume = {8},
	unique-id = {32073571},
	issn = {2307-9266},
	abstract = {The therapeutic effect of multipotent mesenchymal stem cells has been proven on various disease models. One of the mechanisms is the paracrine effect of the cells on the surrounding tissues. The aim. To investigate the secretome effectiveness of the multipotent mesenchymal stem cells in the treatment of adjuvant arthritis and contact-allergic dermatitis in Wistar rats. Materials and methods. Adjuvant arthritis was simulated in 26 female rats by the administration of Freund's complete adjuvant and then treated with the administration of 100 mu l of multipotent mesenchymal stem cell secretome or saline. Contact-allergic dermatitis was modeled on 30 female rats by applying 200 mu l of an oil solution of dinitrofluorobenzene to the skin on days 1, 5 and 6. Then the rats were treated with fluocinolone ointment (a positive control), baby cream (a negative control), baby cream with a secretome of native multipotent mesenchymal stem cells or from the cells processed with dexamethasone. Results. Judging by the indicators of the longitudinal and transverse dimensions of the paws in rats and a histological examination, the secretome did not have any anti-inflammatory effect on adjuvant arthritis. A cream with a secretome from multipotent mesenchymal stem cells processed with dexamethasone, was the most effective on the model of contact-allergic dermatitis: the clinical improvement occurred on the 2nd day. The secretome from native multipotent mesenchymal stem cells and fluocinolone had a therapeutic effect on the 3rd day of application, the negative control - on the 4th day. The lymphocytic infiltration coefficient was significantly lower (p<0.05) in all the cases compared to the negative control (2.8 +/- 0.1). However, the lowest infiltration was observed when the cream with secretome from native (1.75 +/- 0.1) and dexamethasone-stimulated (1.76 +/- 0.1) multipotent mesenchymal stem cells was being used. Conclusion. The cream with the secretome of multipotent mesenchymal stem cells suppresses lymphocytic infiltration more strongly than the highly active topical glucocorticosteroid - fluocinolone - on the model of contact-allergic dermatitis, which is a classic local delayed-type hypersensitivity reaction. However, a further study of the therapeutic effect of the secretome on models of systemic inflammatory diseases is required after its preliminary purification from large-molecular proteins.},
	keywords = {Inflammation; SECRETION; Stem Cells; ADJUVANT ARTHRITIS},
	year = {2020},
	eissn = {2413-2241},
	pages = {416-425}
}

@article{MTMT:31824428,
	title = {Human Mesenchymal Stem Cells: The Present Alternative for High-Incidence Diseases, even SARS-Cov-2},
	url = {https://m2.mtmt.hu/api/publication/31824428},
	author = {Juárez-Navarro, K.J. and Padilla-Camberos, E. and Díaz, N.F. and Miranda-Altamirano, A. and Díaz-Martínez, N.E.},
	doi = {10.1155/2020/8892189},
	journal-iso = {STEM CELLS INT},
	journal = {STEM CELLS INTERNATIONAL},
	volume = {2020},
	unique-id = {31824428},
	issn = {1687-966X},
	abstract = {Mesenchymal stem cells (MSCs), defined as plastic adherent cells with multipotent differentiation capacity in vitro, are an emerging and valuable tool to treat a plethora of diseases due to their therapeutic mechanisms such as their paracrine activity, mitochondrial and organelle transfer, and transfer of therapeutic molecules via exosomes. Nowadays, there are more than a thousand registered clinical trials related to MSC application around the world, highlighting MSC role on difficult-to-treat high-incidence diseases such as the current COVID-19, HIV infections, and autoimmune and metabolic diseases. Here, we summarize a general overview of MSCs and their therapeutic mechanisms; also, we discuss some of the novel clinical trial protocols and their results as well as a comparison between the number of registries, countries, and search portals. © 2020 Karen J. Juárez-Navarro et al.},
	year = {2020},
	eissn = {1687-9678}
}

@article{MTMT:31432181,
	title = {Immunosuppressive Property of MSCs Mediated by Cell Surface Receptors},
	url = {https://m2.mtmt.hu/api/publication/31432181},
	author = {Liu, Siyu and Liu, Fei and Zhou, You and Jin, Baeku and Sun, Qiang and Guo, Shu},
	doi = {10.3389/fimmu.2020.01076},
	journal-iso = {FRONT IMMUNOL},
	journal = {FRONTIERS IN IMMUNOLOGY},
	volume = {11},
	unique-id = {31432181},
	issn = {1664-3224},
	year = {2020},
	eissn = {1664-3224}
}

@article{MTMT:31405452,
	title = {Galectins and their involvement in ocular disease and development},
	url = {https://m2.mtmt.hu/api/publication/31405452},
	author = {Luis, J. and Eastlake, K. and Khaw, P.T. and Limb, G.A.},
	doi = {10.1016/j.exer.2020.108120},
	journal-iso = {EXP EYE RES},
	journal = {EXPERIMENTAL EYE RESEARCH},
	volume = {197},
	unique-id = {31405452},
	issn = {0014-4835},
	keywords = {LIGAND; signal transduction; Pathogenesis; review; human; Tissue regeneration; priority journal; nonhuman; PROTEIN FUNCTION; cell activation; molecular interaction; galectin; galectin; Ophthalmology; glaucoma; eye disease; systemic disease; cornea disease; Retina development},
	year = {2020},
	eissn = {1096-0007}
}

@article{MTMT:31316898,
	title = {Comparative immunomodulatory properties of mesenchymal stem cells derived from human breast tumor and normal breast adipose tissue},
	url = {https://m2.mtmt.hu/api/publication/31316898},
	author = {Sepehr, Koushan Sineh and Razavi, Alireza and Hassan, Zuhair Mohammad and Fazel, Abdolreza and Abdollahpour-Alitappeh, Meghdad and Mossahebi-Mohammadi, Majid and Yekaninejad, Mir Saeed and Farhadihosseinabadi, Behrouz and Hashemi, Seyed Mahmoud},
	doi = {10.1007/s00262-020-02567-y},
	journal-iso = {CANCER IMMUNOL IMMUN},
	journal = {CANCER IMMUNOLOGY IMMUNOTHERAPY},
	volume = {69},
	unique-id = {31316898},
	issn = {1432-0851},
	keywords = {PROLIFERATION; CANCER CELLS; MIGRATION; Galectin-1; Stromal Cells; Oncology; breast cancer; REGULATORY T-CELLS; Mesenchymal stem cells (MSCs)},
	year = {2020},
	eissn = {0340-7004},
	pages = {1841-1854}
}

@article{MTMT:3190069,
	title = {Systemic lupus erythematosus in the light of the regulatory effects of galectin-1 on T-cell function},
	url = {https://m2.mtmt.hu/api/publication/3190069},
	author = {Hornung, Ákos and Monostori, Éva and Kovács, László},
	doi = {10.1177/0961203316686846},
	journal-iso = {LUPUS},
	journal = {LUPUS},
	volume = {26},
	unique-id = {3190069},
	issn = {0961-2033},
	abstract = {Galectin-1 is an endogenous immunoregulatory lectin-type protein. Its most important effects are the inhibition of the differentiation and cytokine production of Th1 and Th17 cells, and the induction of apoptosis of activated T-cells. Galectin-1 has been identified as a key molecule in antitumor immune surveillance, and data are accumulating about the pathogenic role of its deficiency, and the beneficial effects of its administration in various autoimmune disease models. Initial animal and human studies strongly suggest deficiencies in both galectin-1 production and responsiveness in systemic lupus erythematosus (SLE) T-cells. Since lupus features widespread abnormalities in T-cell activation, differentiation and viability, in this review the authors wished to highlight potential points in T-cell signalling processes that may be influenced by galectin-1. These points include GM-1 ganglioside-mediated lipid raft aggregation, early activation signalling steps involving p56Lck, the exchange of the CD3 zeta-ZAP-70 to the FcRgamma-Syk pathway, defective mitogen-activated protein kinase pathway activation, impaired regulatory T-cell function, the failure to suppress the activity of interleukin 17 (IL-17) producing T-cells, and decreased suppression of the PI3K-mTOR pathway by phosphatase and tensin homolog (PTEN). These findings place galectin-1 into the group of potential pathogenic molecules in SLE.},
	year = {2017},
	eissn = {1477-0962},
	pages = {339-347},
	orcid-numbers = {Monostori, Éva/0000-0002-7442-3562; Kovács, László/0000-0003-4457-1430}
}

@article{MTMT:27049125,
	title = {Galectin-1 and galectin-3 expression in equine mesenchymal stromal cells (MSCs), synovial fibroblasts and chondrocytes, and the effect of inflammation on MSC motility},
	url = {https://m2.mtmt.hu/api/publication/27049125},
	author = {Reesink, Heidi L and Sutton, Ryan M and Shurer, Carolyn R and Peterson, Ryan P and Tan, Julie S and Su, Jin and Paszek, Matthew J and Nixon, Alan J},
	doi = {10.1186/s13287-017-0691-2},
	journal-iso = {STEM CELL RES THER},
	journal = {STEM CELL RESEARCH & THERAPY},
	volume = {8},
	unique-id = {27049125},
	issn = {1757-6512},
	year = {2017},
	eissn = {1757-6512}
}

@article{MTMT:3110431,
	title = {The role of extracellular vesicle and tunneling nanotube-mediated intercellular cross-talk between mesenchymal stem cells and human peripheral T cells.},
	url = {https://m2.mtmt.hu/api/publication/3110431},
	author = {Matula, Zsolt and Németh, Andrea and Lőrincz, Péter and Szepesi, Áron and Brózik, Anna and Buzás, Edit Irén and Lőw, Péter and Német, Katalin and Uher, Ferenc and Suhajdáné Urbán, Veronika},
	doi = {10.1089/scd.2016.0086},
	journal-iso = {STEM CELLS DEV},
	journal = {STEM CELLS AND DEVELOPMENT},
	volume = {25},
	unique-id = {3110431},
	issn = {1547-3287},
	abstract = {The role of extracellular vesicles in mediating the immunosuppressory properties of mesenchymal stem cells has recently attracted remarkable scientific interest. The aim of this work was to analyze the transport mechanisms of membrane and cytoplasmic components between T lymphocytes and adipose tissue-derived mesenchymal stem cells, by focusing on the role of distinct populations of extracellular vesicles, direct cell-cell contacts and the soluble mediators per se in modulating T lymphocyte function. We found that neither murine thymocytes and human primary T cells, nor Jurkat lymphoblastoid cells incorporated appreciable amounts of MSC-derived microvesicles or exosomes. Moreover, these particles had no effect on the proliferation and IFN-gamma production of in vitro stimulated primary T cells. In contrast, AD-MSCs incorporated large amounts of membrane components from T cells as an intensive uptake of exosomes and microvesicles could be observed. Interestingly, we found a bi-directional exchange of cytoplasmic components between human AD-MSCs and primary T lymphocytes, mediated by tunneling nanotubes derived exclusively from the T cells. In contrast, tunneling nanotubes couldn't be observed between AD-MSCs and the Jurkat cells. Our results reveal a novel and efficient way of intercellular communication between MSCs and T cells, and may help a better understanding of the immunomodulatory function of MSCs.},
	year = {2016},
	eissn = {1557-8534},
	pages = {1818-1832},
	orcid-numbers = {Németh, Andrea/0000-0002-0015-8436; Lőrincz, Péter/0000-0001-7374-667X; Buzás, Edit Irén/0000-0002-3744-206X; Lőw, Péter/0000-0003-2450-7087; Uher, Ferenc/0000-0001-7997-6142; Suhajdáné Urbán, Veronika/0000-0003-0393-5891}
}

@article{MTMT:31390785,
	title = {Mechanisms of immunosuppression by mesenchymal stromal cells: a review with a focus on molecules},
	url = {https://m2.mtmt.hu/api/publication/31390785},
	author = {Nishizawa, Kazuhisa and Seki, Reiko},
	doi = {10.15761/BRCP.1000116},
	journal-iso = {Biomed Res Clin Prac},
	journal = {Biomedical Research and Clinical Practice},
	volume = {1},
	unique-id = {31390785},
	year = {2016},
	eissn = {2397-9631},
	pages = {82-96}
}