Publications by authors named "Mercedes Lopez-Santalla"

Rheumatoid arthritis (RA) is an autoimmune disease characterized by synovial hyperplasia and cartilage/bone destruction with systemic comorbidities. Despite advances in understanding the aetiology of RA and novel biologic drugs, a substantial number of individuals with RA remain intolerant or resistant to these therapies. In this context, mesenchymal stem/stromal cell (MSC)-based therapy has emerged as an innovative therapeutic alternative to address unresolved treatment issues for patients with RA thanks to the immunomodulatory properties of these cells.

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Inflammatory bowel diseases (IBD) consisting of persistent and relapsing inflammatory processes of the intestinal mucosa are caused by genetic, environmental, and commensal microbiota factors. Despite recent advances in clinical treatments aiming to decrease inflammation, nearly 30% of patients treated with biologicals experienced drawbacks including loss of response, while others can develop severe side effects. Hence, novel effective treatments are highly needed.

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Galectin-1 is a -galactoside-binding lectin, ubiquitously expressed in stromal, epithelial, and different subsets of immune cells. Galectin-1 is the prototype member of the galectin family which shares specificity with -galactoside containing proteins and lipids. Immunomodulatory functions have been ascribed to endogenous galectin-1 due to its induction of T cell apoptosis, inhibitory effects of neutrophils and T cell trafficking.

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Rheumatoid arthritis (RA) is a chronic systemic autoimmune disease characterized by synovial inflammation and progressive joint destruction and is a primary cause of disability worldwide. Despite the existence of numerous anti-rheumatic drugs, a significant number of patients with RA do not respond or are intolerant to current treatments. Mesenchymal stem/stromal cell (MSCs) therapy represents a promising therapeutic tool to treat RA, mainly attributable to the immunomodulatory effects of these cells.

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Rheumatoid arthritis (RA) is a chronic systemic autoimmune disease that affects the lining of the synovial joints leading to stiffness, pain, inflammation, loss of mobility, and erosion of joints. Its pathogenesis is related to aberrant immune responses against the synovium. Dysfunction of innate and adaptive immunity, including dysregulated cytokine networks and immune complex-mediated complement activation, are involved in the progression of RA.

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Background And Aims: Mesenchymal stem cells [MSCs] are used in preclinical and clinical studies for treatment of immune-mediated disorders, thanks to their immunomodulatory properties. Cell therapy with MSCs induces multiple effects in the immune system which ultimately lead to increase in the number of immune cells with regulatory phenotype. In this study, we investigated whether the beneficial effects of MSC therapy are maintained in the long term in a clinically relevant mouse model of colitis.

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Nanoparticles derived from the elongated flexuous capsids of (TuMV) have been shown to be efficient tools for antibody sensing with a very high sensitivity if adequately functionalized with the corresponding epitopes. Taking advantage of this possibility, TuMV virus-like particles (VLPs) have been genetically derivatized with a peptide from the chaperonin Hsp60, a protein described to be involved in inflammation processes and autoimmune diseases. Antibodies against the peptide have been previously shown to have a diagnostic value in at least one autoimmune disease, multiple sclerosis.

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Mesenchymal stem cells (MSCs) have emerged as a promising treatment for inflammatory diseases. The immunomodulatory effect of MSCs takes place both by direct cell-to-cell contact and by means of soluble factors that leads to an increased accumulation of regulatory immune cells at the sites of inflammation. Similar efficacy of MSCs has been described regardless of the route of administration used, the inflammation conditions and the major histocompatibility complex context.

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Evidence indicates an intimate connection between the neuroendocrine and the immune systems. A number of and studies have demonstrated growth hormone (GH) involvement in immune regulation. The GH receptor is expressed by several leukocyte subpopulations, and GH modulates immune cell proliferation and activity.

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Mesenchymal stem cells (MSCs) have a large potential in cell therapy for treatment of inflammatory and autoimmune diseases, thanks to their immunomodulatory properties. The encouraging results in animal models have initiated the translation of MSC therapy to clinical trials. In cell therapy protocols with MSCs, administered intravenously, several studies have shown that a small proportion of infused MSCs can traffic to the draining lymph nodes (LNs).

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Mesenchymal stem cells (MSCs) are multipotent stromal cells with immunomodulatory properties. They have emerged as a very promising treatment for autoimmunity and inflammatory diseases such as rheumatoid arthritis. Previous studies have demonstrated that MSCs, administered systemically, migrate to lymphoid tissues associated with the inflammatory site where functional MSC-induced immune cells with a regulatory phenotype were increased mediating the immunomodulatory effects of MSCs.

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Modulation of innate immune responses in rheumatoid arthritis and other immune-mediated disorders is of critical importance in the clinic since a growing body of information has shown the key contribution of dysregulated innate responses in the progression of the disease. Mesenchymal stromal cells (MSCs) are the focus of intensive efforts worldwide due to their key role in tissue regeneration and modulation of inflammation. In this study, we define innate immune responses occurring during the early course of treatment with a single dose of expanded adipose-derived MSCs (eASCs) in established collagen-induced arthritis.

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Objective: The T allele of rs7574865 in STAT4 confers risk of developing autoimmune disorders. However, its functional significance remains unclear. Here we analyze how rs7574865 affects the transcription of STAT4 and its protein expression.

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Article Synopsis
  • Mesenchymal stem cells (MSCs) are promising candidates for treating autoimmune and inflammatory diseases, like rheumatoid arthritis, due to their ability to suppress inflammation.
  • A study showed that administering human adipose-derived MSCs (eASCs) to mice with arthritis significantly reduced disease severity and decreased pathogenic GM-CSF-expressing CD4 T cells.
  • The treatment also increased various regulatory T cell subsets in the lymph nodes, indicating a shift towards a better balance between regulatory and inflammatory cells, which suggests a potential therapeutic role for eASCs in managing arthritis.
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Objective: The p38 MAPK is important in the pathogenic immune response in rheumatoid arthritis (RA). The p38 molecule can be activated through phosphorylation on Thr¹⁸⁰-Tyr¹⁸² by upstream MAPK kinases and via an alternative pathway through phosphorylation on Tyr³²³. We undertook this study to quantify the phosphorylation of Tyr³²³ p38 and of Thr¹⁸⁰-Tyr¹⁸² p38 on T cells from healthy controls and patients with RA or ankylosing spondylitis (AS) to identify variables associated with p38 phosphorylation and disease activity.

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  • - The study examined T lymphocytes from gastric cancer patients using a specific virus transformation technique to create T-cell lines for analysis of their function and characteristics.
  • - Results showed that these T cells had significantly lower responses to stimulation from certain antibodies and interleukins compared to healthy controls, indicating impaired function in the cancer patients.
  • - The findings suggest that dysfunctional mucosal T lymphocytes in gastric adenocarcinoma patients may hinder the body's ability to control tumor growth effectively.
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  • Defective CD3zeta chain expression is noted in T lymphocytes of patients with inflammatory diseases and cancers, yet its role in cancer is less understood compared to conditions like lupus.
  • This study examined T lymphocytes from gastric adenocarcinoma patients and found that the absent CD3zeta chain was not replaced by FcRgamma, unlike in lupus patients.
  • The altered expression of signaling molecules in cancer T lymphocytes may explain their reduced ability to proliferate, with T-cell lines serving as useful tools for further investigation.
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  • Low expression of the CD3zeta chain in T cells is linked to cancer, specifically observed in patients with gastric adenocarcinoma, suggesting that it may affect the immune response.
  • A study measured CD3zeta and CD3epsilon levels in T-cell lines from cancer patients and healthy volunteers, finding that CD3zeta was significantly reduced, independent of tumor-derived factors.
  • This downregulation of CD3zeta in T cells could hinder their ability to effectively combat tumor growth, indicating an inherent characteristic of cancer patient cells rather than a response to external tumor influences.
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  • A study on 25 patients with resectable gastric adenocarcinoma illustrated differences in immune response between patients with and without residual neoplastic disease (RND- vs. RND+).
  • Both patient groups had significantly fewer CD3-expressing cells compared to healthy individuals, indicating a compromised immune response.
  • The reduced expression of CD45 and poor proliferation of immune cells in RND+ patients may serve as indicators for faster disease progression and could help in determining the need for more aggressive treatment options.
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Objectives: To detect the presence of antibodies against bovine serum albumin in a cohort of Spanish patients with type 1 insulin-dependent diabetes.

Methods: Antibodies were measured using an in-house enzyme-linked immunosorbent assay test in 80 patients with type 1 diabetes, subdivided according to the presence or absence in their serum of celiac disease-related antibodies. For comparison, 30 patients with celiac disease (nondiabetic), 13 patients with autoimmune thyroiditis, and 45 healthy volunteers were used.

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