Browsing by Subject "Monocytes"

Now showing 1 - 3 of 3
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    lnhibited differentiation of Langerhans cells in the rat epidermis upon systemic treatment with cyclosporin A
    (Murcia : F. Hernández, 2001) Borghi-Cirri, M.B.; Riccardi-Arbi, R.; Bacci, S.; Mori, M.; Pimpinelli, N.; Romagnoli, P.; Filipponi, F.
    The immunosuppressant drug cyclosporin A (CsA) is known to cause reduction in number, DNA synthesis and function of Langerhans cells (LC). Since also the differentiation of LC is known to be hampered in conditions of acquired immunodeficiency not due to drugs, we investigated whether this occurs with CsA. Rats were injected subcutaneously with CsA (5, 10 and 50 mg.kg-l.d-l) for three weeks; the skin was analyzed by Ia immunohistochemistry and by electron microscopy. Epidermal immunolabeled cells were 1553.5 (mean I SEM) per 100 basa1 keratinocytes in untreated controls and 8.7511.3, 4.7551.0 and 1.751.2 upon increasing doses of CsA (pe0.01). By electron microscopy, monocytoid cells with deep invaginations of the plasma membrane and roundish LC poor in Birbeck granules appeared in the epidermis upon treatment. The results suggest that CsA inhibits the differentiation of LC precursors in the epidermis and that this can in part explain the selective increase in the risk of skin vira1 disease and cancer in chronically treated patients.
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    Priming is dispensable for NLRP3 inflammasome activation in human monocytes in vitro
    (Frontiers Media, 2020-09-30) Martín Sánchez, María Rosario Fátima; Gritsenko, Anna; Yu, Shi; Díaz del Olmo, Inés; Nichols, Eva María; Davis, Daniel M.; Brough, David; López Castejón, Gloria; Farmacología
    Interleukin (IL)-18 and IL-1b are potent pro-inflammatory cytokines that contribute toinflammatory conditions such as rheumatoid arthritis and Alzheimer’s disease. They areproduced as inactive precursors that are activated by large macromolecular complexescalled inflammasomes upon sensing damage or pathogenic signals. NLRP3inflammasome activation is regarded to require a priming step that causes NLRP3 andIL-1b gene upregulation, and also NLRP3 post-translational licencing. A subsequentactivation step leads to the assembly of the complex and the cleavage of pro-IL-18 andpro-IL-1b by caspase-1 into their mature forms, allowing their release. Here we show thathuman monocytes, but not monocyte derived macrophages, are able to form canonicalNLRP3 inflammasomes in the absence of priming. NLRP3 activator nigericin caused theprocessing and release of constitutively expressed IL-18 in an unprimed setting. This wasmediated by the canonical NLRP3 inflammasome that was dependent on K + and Cl−efflux and led to ASC oligomerization, caspase-1 and Gasdermin-D (GSDMD) cleavage.IL-18 release was impaired by the NLRP3 inhibitor MCC950 and by the absence ofNLRP3, but also by deficiency of GSDMD, suggesting that pyroptosis is the mechanism ofrelease. This work highlights the readiness of the NLRP3 inflammasome to assemble inthe absence of priming in human monocytes and hence contribute to the very early stagesof the inflammatory response when IL-1b has not yet been produced. It is important toconsider the unprimed setting when researching the mechanisms of NLRP3 activation, asto not overshadow the pathways that occur in the absence of priming stimuli, which mightonly enhance this response.
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    Systemic immune and tumor marker profiles in ovarian and deep infiltrating endometriosis: associations with disease severity and symptom burden
    (MDPI, 2025-10-01) Marín Sánchez, Pilar; Nebot, Ana; García-Izquierdo, Laura; Nieto-Meca, Lucía; Sánchez, Rocío; Machado Linde, Francisco; Martínez-Esparza Alvargonzález, María Concepción; Ramírez Pávez, Tamara Nadira; Bioquímica y Biología Molecular B e Inmunología; Facultad de Medicina
    Endometriosis is a chronic, estrogen-dependent inflammatory disease with heterogeneous clinical manifestations and uncertain systemic immune involvement. This study aimed to characterize peripheral immune profiles and circulating tumor markers in women with ovarian endometrioma (OE) and deep infiltrating endometriosis (DIE), and to explore their associations with disease severity, symptom burden, and physical health perception. Peripheral blood leukocyte subsets, plasma cytokines, and tumor markers (CA125, CA19-9, CEA, HE4) were analyzed in 146 patients and 50 healthy controls. OE was associated with increased monocyte counts and reduced neutrophil proportions, while DIE showed elevated levels of IL-8 and Galectin-1. IL-33 levels correlated negatively with the revised American Society for Reproductive Medicine (rASRM) scores and positively with neutrophil proportion, suggesting a role in systemic immune regulation. Tumor marker levels varied by subtype: CA19-9 was higher in OE, and CEA in DIE. CA125 correlated with disease severity, and CEA with monocyte levels. Exploratory heatmaps revealed consistent immune-tumor associations linked to anatomical severity and symptom profiles. Although exploratory, these findings highlight the presence of distinct systemic immune patterns in endometriosis and support the potential of integrative blood-based biomarkers for future diagnostic and stratification strategies.