Browsing by Subject "Dendritic cells"
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- PublicationOpen AccessAn overview of the structural and functional aspects of immune cells in teleosts(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2021) Mokhtar, Doaa M.; Abdelhafez, Enas A.The immune system of fish consists of two main components, innate and adaptive immunities. Innate immunity is non-specific and acts as the primary line of protection against pathogen invasion, while adaptive immunity is more specific to a certain pathogen/following adaptation. The adaptive immune system consists of the humoral and cellular components. Cytotoxic T-lymphocyte cells are the major component of the cellular immunity that frequently kills viral-, bacterial- or parasitic-infected cells. According to the anatomical location, the mucosal-associated lymphoid tissue (MALT) in teleost fish subdivides into gutassociated lymphoid tissue (GALT), gill-associated lymphoid tissue (GIALT), and skin-associated lymphoid tissue (SALT). The MALTs contain various leukocytes; including, but not limited to, lymphocytes (T and B cells), plasma cells, macrophages, and granulocytes. Macrophages are multifunctional cells that are mainly involved in the immune response, including; phagocytosis and degradation of foreign antigens, tissue remodeling, and production of cytokines, chemokines and growth factors. An interesting feature of teleost macrophages is their ability to form melanomacrophage centers (MMC) in the hemopoietic tissues. Dendritic cells, rodlet cells, mast cells, eosinophilic granular cells (ECGs), telocytes, osteoclasts, club cells, as well as, barrier cells have been recorded in many fish species and have many immunological roles. This paper aims to summarize the current knowledge of the immune cells present in fish tissues serving as anatomical and physiological barriers against external hazards. Increased knowledge of fish immune systems will facilitate the development of novel vaccination strategies in fish.
- PublicationOpen AccessAnalysis of the in vivo dend ritic cell response to the bacterial superantigen staphylococcal enterotoxin B in the mouse spleen(F. Hernández y Juan F. Madrid. Universidad de Murcia: Departamento de Biología Celular e Histología, 2001) Yoon, S.; Bae, K. L.; Shin, J. Y.; Yoo, H. J.; Lee, H. W.; Baek, S. Y.; Kim, B. S.; Kim, J. B.; Lee, H. D.To inv esti ga te th e in vi vo effec ts of St
- PublicationOpen AccessBlood-borne cells involved in arterial repair upon experimental incision injury(Murcia : F. Hernández, 2008) Pieri, L.; Rinaldi, B; Domenici Lombardo, L.; Bacci, S.; Filippelli, A.; Capuano, A.; Rossi, F.; Romagnoli, P.Summary. We had previously shown that microscopically detectable infiltration of dendritic cells and expression of Hsp47 in tissue lysates occur during repair upon experimental arterial injury. We have further analysed here the cell types involved in the repair process by histology, electron microscopy and immunofluorescence. Rat carotid arteries were subjected to brief crushing and full thickness incision and were analysed up to 21 d thereafter. Adhesion and activation of platelets occurred 3 h after surgery. A neointima had formed 7 d after surgery, where immature cells entered from the lumen and gave rise to cells rich in organelles of the secretory pathway and endowed with bundles of phalloidin-binding microfilaments. Alpha smooth muscle-positive, secretory and contractile smooth muscle cells were found in the neointima 14 and 21 d after injury. Seven to 21 d after surgery, endothelial cells appeared immature and the newly formed tissue contained MHC-II positive, CD43 positive dendritic cells which clustered with lymphocytes, a few macrophages containing apoptotic remnants and cells labelled for Hsp47. Thin elastic fibrils appeared in the neointima 21 d after injury. The results suggest that the response to acute arterial incision injury is mediated by blood borne cells which differentiate along multiple pathways; the process evolves without reaching stabilization within the observed time lapse; the secretion of extracellular matrix is marked by the expression of Hsp47; and the constant presence of dendritic cells clustered with lymphocytes makes these cells candidate to a pivotal role in the tissue response to injury.
- PublicationOpen AccessComparative analysis of CD1a, S-100, CD83, and CD11c human dendritic cells in normal, premalignant, and malignant tissues(Murcia : F. Hernández, 2005) Perez, L.; Shurin, M.R.; Kogan, D.; Tourkova, I.L.; Shurin, G.V.; Collins, B.A number of antibodies that recognize human dendritic cells (DC) have been identified. The main aim of this study was to compare and contrast different antigen retrieval techniques using both enzymatic and non-enzymatic treatments in order to determine the expression and distribution of several DC markers on formalin-fixed, paraffin-embedded tissues. Normal human lung, oral epithelial hyperplasia lesions, oral squamous cell carcinoma, and prostate adenocarcinoma tissues were evaluated using a panel of DC specific antibodies. The results of immunohistochemical staining for CD83, CD1a, CD11c, and S-100 DC markers were compared following the different antigen retrieval approaches. The overall best results for the analysis of tumor-associated DC were obtained with the enzymatic methods. Protease XXIV digestion was determined to be essential for detection of S-100 and CD11c positive DC, whereas trypsin and pepsin were required for the recognition of CD1a and CD83 expressing tumor-associated DC. These results could be easily adapted for routine practice and should be useful for characterization of the DC system in cancer patients for both diagnostic and prognostic purposes. In addition, standardized procedures for evaluating different subpopulations of tumor-associated DC should bring new insights in understanding of DC-tumor cell interaction.
- PublicationOpen AccessDendritic cell migration and lymphocyte homing imprinting(Murcia : F. Hernández, 2008) Villablanca, Eduardo J.; Russo, Vicenzo; Rodrigo Mora, J.For an effective adaptive immune response to occur, dendritic cells (DC), which are the most efficient antigen-presenting cells, must be able to sample the peripheral microenvironment and migrate towards secondary lymphoid organs (SLO) where they activate naïve lymphocytes. Upon activation, lymphocytes proliferate and acquire the capacity to migrate to extralymphoid compartments. Although the molecular mechanisms controlling lymphocyte homing to lymphoid and to some extralymphoid tissues have been described in significant detail, it is much less clear how DC migration is controlled. Do DC obey similar adhesion cues that lymphocytes do, or do they have their own “zip codes”? This is relevant from a therapeutic standpoint because effective DC-based vaccines should be able to reach the appropriate tissues in order to generate protective immune responses. Here, we discuss some of the mechanisms used by DC to reach their target tissues. Once DC arrive at their destination, they are exposed to the tissue microenvironment, which likely modulates their functional properties in a tissue-specific fashion. This local DC “education” is probably responsible among other things; for the acquisition of tissue-specific homing imprinting capacity by which DC instruct lymphocytes to migrate to specific tissues. Finally, we discuss how dysregulation of these signals may play a key role in disease.
- PublicationOpen AccessDendritic cells, sentinels against pathogens(Murcia : F. Hernández, 2004) Chung, N.P.I.; Chen, Y.; Chan, Vera S.F.; Tam, P.K.H.; Lin, C.L.S.Dendritic cells (DCs) are the most potent antigen-presenting cells, and are regarded as “natural adjuvants” for the induction of primary T or T-dependent immunity. DCs in the peripheral sites capture and process antigens. Encounter of exogenous or endogenous stimuli mature the function of DCs, and they thus acquire T-cell stimulatory capacity and distinct chemotactic behavior which enables them to migrate to lymphoid tissue. In the secondary lymphoid organs, they present antigens to T- and B-cells and stimulate their proliferation. Dendritic cells are also involved in tolerance induction, in particular, to self antigens. DCs also play a key role in the transmission of many pathogens, and therefore may become targets for designing new therapies. DCs have been manipulated in vitro and in vivo for cancer immunotherapy. In this article, we provide a concise overview of DC biology and its current and future role in clinical settings.
- PublicationOpen AccessDistribution of dendritic cells expressing dendritic cell-specific ICAM-3-grabbing non-integrin (DC-SIGN, CD209): Morphological analysis using a novel Photoshop-aided multiple immunohistochemistry technique(F. Hernández y Juan F. Madrid. Universidad de Murcia: Departamento de Biología Celular e Histología, 2014) Masuda, Akihiro; Nishikawa, ToshioThe distribution of dendritic cells (DCs) expressing DC-specific ICAM-3-grabbing non-integrin (DC-SIGN, CD209) and the morphological interaction of DC-SIGN+ DCs with other cells, especially B cells, in tonsillar and other lymphoid tissues were investigated by multiple immunohistochemistry (IHC) using the graphics editing program Photoshop, which enabled staining with 4 or more antibodies in formalin-fixed paraffin sections. Images obtained by repetition of conventional IHC using diaminobenzidine color development in a tissue section were processed on Photoshop for multiple staining. DC-SIGN+ DCs were present in the area around the lymphoid follicles and formed a DC-SIGN+ DC-rich area, and these cells contacted not only T cells, fascin+ DCs, and blood vessels but also several subsets of B cells simultaneously, including naïve and memory B cells. DC-SIGN+ DCs may play an important role in the regulation of the immune response mediated by not only T cells but also B cells. The multiple IHC method introduced in the present study is a simple and useful method for analyzing details of complex structures. Because this method can be applied to routinely processed paraffin sections with conventional IHC with diaminobenzidine, it can be applied to a wide variety of archival specimens.
- PublicationOpen AccessEvidence that dendritic cells infiltrate atherosclerotic lesions in apolipoprotein E-deficient mice(Murcia : F. Hernández, 2001) Bobryshev, Y.V.; Taksir, T.; Freeman, M.W.Earlier we reported that atherosclerotic lesions of apoE-deficient mice contained cells which stained positively with anti-S-100 antibody and that cells exhibiting the ultrastructural features of dendritic cells were present in the aortic lesions. These observations suggested that dendritic cells might be involved in mouse atherosclerosis. By employing DEC-205 and MIDC-8 antibodies specific for dendritic cells, the present study has established that dendritic cells indeed accumulate in atherosclerotic lesions of apoE-deficient mice. Finding dendritic cells infiltrating atherosclerotic lesions in apoE-deficient mice offers the possibility of investigating the migratory routes of dendritic cells and their involvement in T-cell activation.
- PublicationOpen AccessGlucocorticoid receptor modulates dendritic cell function in ulcerative colitis(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2020) Yang, Xinxin; Geng, JingshuUlcerative colitis (UC) is a serious form of inflammatory bowel disease (IBD) occurring worldwide. Although anti-TNF therapy is found to be effective in over 70% of patients with UC, nearly one-third are still deprived of effective treatment. Because glucocorticoids (GC) can effectively inhibit granulocyte-recruitment into the mucosa, cytokine secretion and T cell activation, they are used widely in the treatment of UC. However, remission is observed in only 55% of the patients after one year of steroid use due to a condition known as steroid response. Additionally, it has been noted that 20%-40% of the patients with UC do not respond to GC treatment. Researchers have revealed that the number of dendritic cells (DCs) in patients with UC tends to increase in the colonic mucosa. Many studies have determined that the removal of peripheral DCs through the adsorption and separation of granulocytes and monocytes could improve tolerance of the intestine to its symbiotic flora. Based on these results, further insights regarding the beneficial effects of Adacolumn apheresis in patients subjected to this treatment could be revealed. GC can effectively inhibit the activation of DCs by reducing the levels of major histocompatibility complex class II (MHC II) molecules, which is critical for controlling the recruitment of granulocytes. Therefore, alternative biological and new individualized therapies based on these approaches need to be evaluated to counter UC. In this review, progress in research associated with the regulatory effect of glucocorticoid receptors on DCs under conditions of UC is discussed, thus providing insights and identifying potential targets which could be employed in the treatment strategies against UC
- PublicationOpen AccessIn-situ analysis of mast cells and dendritic cells in coronary atherosclerosis in chronic kidney disease (CKD)(Universidad de Murcia. Departamento de Biología Celular e Histología, 2018) Wachter, D.L.; Neureiter, Daniel; Câmpean, V.; Hilgers, K.F.; Büttner Herold, M.; Daniel, C.; Benz, K.; Amann, K.Aims. Mast cells (MC) and dendritic cells (DC) have immune modulatory function and can influence T-cell activity. Both cell types have been found in atherosclerotic plaques and are thought to play an important role for plaque stability. Compared to matched segments of the non-renal population, patients with chronic kidney disease (CKD) show a more pronounced and more aggressive course of atherosclerosis with higher plaque calcification and significantly higher complication rates. It was the aim of this study to analyze the number and localization of MCs and DCs, macrophages, T- and B-cells as well as the expression of markers of inflammation such as CRP and NFκΒ in calcified and non-calcified atherosclerotic plaques of patients with CKD and control patients. Methods. Fifty coronary atherosclerotic plaques from patients with endstage CKD (CKD, n=25) and control (n=25) patients were categorized according to the Stary classification and investigated using immunohistochemistry (markers for MC, DC, T, B, macrophage and NFκΒ). Expression was analyzed separately for the complete plaque area as well as for the different plaque subregions and correlations were analyzed. Results. We found only very few DCs and MCs per lesion area with slightly increased numbers in calcified plaques. MCs per plaque area were significantly more frequent in CKD than in control patients and this was independent of plaque calcification. MCs were most frequently found in the shoulder and basis of the plaque. DCs per plaque area were significantly less in calcified plaques of CKD compared to control patients. In control, but not in CKD patients, DCs were significantly more frequent in calcified than in non-calcified plaques. Within the plaques, DCs were similarly distributed between all 4 subregions. Conclusions. Coronary atherosclerotic plaques of CKD patients showed a significantly higher number of MCs whereas DCs were less frequent compared to control patients particularly if plaques were calcified. These findings might indicate a potential proinflammatory role of MCs, but not of DCs in atherosclerotic lesions of CKD patients, adding another characteristic of advanced atherosclerosis in these patients.
- PublicationOpen AccessInhibition of dendritic cell autophagy alleviates the progression of allergic rhinitis by inhibiting Th1/Th2/Th17 immune imbalance and inflammation(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2025) Xiao, Changwu; Feng, Lizhi; Yang, WeiIntroduction. Immune imbalance is a fundamental immunological feature of allergic rhinitis (AR). The autophagy in CD11c+ dendritic cells (DCs), the strongest antigen-presenting cells, was reported to induce the occurrence of AR by facilitating CD4+ T cell immune imbalance and subsequent inflammation. Our study was designed to confirm that inhibition of DC autophagy can alleviate the progression of AR by inhibiting the T cell immune imbalance. Methods. The AR mouse model was established by using ovalbumin (OVA). OVA-induced mouse models were then injected intraperitoneally with the autophagy inhibitor Baf-A1. Levels of OVA-specific IgE, PGD2, ECP, LTC4, and Th1/Th2/Th17 cell-related cytokines in serum or nasal lavage fluid (NLF) were examined using the corresponding commercial ELISA kits. Morphological changes in the nasal mucosa were observed by HE staining. Nasal mucosa tissues were collected for western blotting to assess the expression of autophagy markers (LC3, P62, and Beclin 1) in each group of mice. Results. Baf-A1 treatment alleviated the allergic symptoms, mitigated inflammatory immune cell infiltration in the nasal mucosa, decreased IgE, LTC4, ECP, and PGD2 levels in both serum and NLF, impaired CD11c+ DC autophagy, and restored Th1/Th2/Th17 cytokine imbalance in OVA-induced AR mice. Furthermore, Baf-A1 treatment also reversed the immune imbalance of CD4+ T cell subtypes and attenuated Th1/Th2/Th17 cytokine imbalance in vitro. Conclusion. Inhibition of CD11c+ DC autophagy suppressed the immune imbalance of CD4+ T cell subsets and attenuated the subsequent inflammatory response, thereby ameliorating the progression of AR.
- PublicationOpen Accesslnsulitis and islet microvasculature in type 1 diabetes(Murcia : F. Hernández, 1993) Papaccio, G.Type 1 diabetes is characterized by a mononuclear infiltration, commonly called «insulitis». The cells that constitute the insulitis are mainly monocytes that are recruited from extraislet areas and arrive at the islet site via the vascular system. Infiltrating cells must then pass across the endothelia to gain access to the islet parenchyma. The anatomy and physiology of the islet microvasculature shows that islet B cells are firstly perfused and influence both endocrine non-B islet cells and periinsular exocrine cells. The low dose streptozocin (LDS) treatment is able to induce, other than a monocyte/macrophage recruitment and activation, islet vascular alterations, mainly at the leve1 of post-capillary venules encircling the islets of Langerhans and a concomitant fa11 in Superoxidedismutase (SOD) (the first cellular defence against free radicals) activity. These findings, together with the increase in vascular permeability and the morphological evidence of areas of oedema formation within the islets, have raised the interest in the «microvasculm> approach to this disease. Actually the reduction in B-cell perfusion and the concomitant attack by phagocytes with a fall in SOD activity should be considered as events that are linked to each other. On the other hand both macrophages and endothelia are able to produce free radicals and, in particular, nitric oxide. This confirms that the islet vascular system seems to be involved in early insulitis and B-cell lysis.
- PublicationOpen AccessMyeloid cell distribution and activity in multiple sclerosis(Universidad de Murcia. Departamento de Biología Celular e Histología, 2016) Moliné-Velázquez, Verónica; Vila-del Sol, Virginia; de Castro, Fernando; Clemente, DiegoMultiple sclerosis (MS) is a demyelinating disease in which an exacerbated immune response provokes oligodendrocyte loss and demyelination, the hallmarks of this neurological disease. The destruction of myelin due to the uncontrolled activity of the invading immune cells leads to the formation of MS plaques. Among the different leukocytes that participate in the immune response associated with MS, the role of myeloid cells has been analyzed extensively (i.e. macrophages, dendritic cells -DCs- and neutrophils). Hence, in this review we will summarize what is known about the distribution, expression and markers available to study myeloid cells, and their histopathology, not only in a standard animal model of MS (autoimmune experimental encephalomyelitis -EAE) but also in MS tissue. In this review, we will not only refer to mature myeloid cells but also to the undifferentiated and almost unexplored myeloid-derived suppressor cells (MDSCs). The active role of MDSCs in the prompt resolution of an immune episode is gaining importance, yet is still the subject of some debate. Finally, the similarities and differences between MS and EAE are discussed, particularly in terms of myeloid cell phenotype, activity and the markers used.
- PublicationOpen AccessThe role of dendritic cells in immune regulation of nasal polyps(Universidad de Murcia. Departamento de Biología Celular e Histología, 2017) Liang, Zhuoping; Yang, Ting; Xu, Wei; Huang, Ying; Jiang, Liang; Yin, Zedeng; Qin, GangNasal polyps (NPs) are caused by a variety of immune cells and inflammatory cells. However, as the most potent antigen-presenting cells in the immune system, the role of dendritic cells (DCs) in NPs is still unclear. In the present research, we studied the role of DCs in immune regulation of NPs. Thirty patients with NPs, who served as the experimental group, received systemic and local glucocorticoids for 4-7 d, and specimens were collected prior to hormone treatment and during surgery. Normal middle turbinate mucosa tissues from 18 patients who underwent nasal septum surgery were collected as controls. The expression levels of CD83, tumor necrosis factor-α (TNF-α), interleukin-4 (IL-4) and eosinophils (EOS) in NP tissues before and after glucocorticoid therapy and in control middle turbinate mucosa tissues were studied. After glucocorticoid therapy, the expression levels of CD83, TNF-α, IL-4 and EOS decreased significantly. In addition, the expression of IL-4 was lower than that of TNF-α, reversing the Th2 cytokine-dominant condition. CD83 and EOS showed a positive correlation. DCs participated in the development and progression of NPs and could promote the generation of Th2 cytokines. After interference by glucocorticoid therapy, DCs could inhibit the expression of Th2 cytokines and induce secretion of Th1 cytokines. DCs and EOS thus might both play roles in promoting the development and progression of NPs, but the underlying mechanism requires further study.
- PublicationOpen AccessTumoricidal potential of binary therapy in lymphoma: Role of DC-NK cross-talk and checkpoint inhibitors(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2025) Chaudhary, Pratima; Yadav, Pragya; Manna, Partha Pratim; Biología Celular e HistologíaLymphoma is a common type of cancer that occurs in humans. Diffuse large B-cell lymphoma (DLBCL) is the most common non-Hodgkin lymphoma (NHL) subtype and is characterized by high clinical and biological heterogeneity. The tumor microenvironment (TME) in lymphoma is critical for the initiation, progression, and metastasis of tumors and influences the therapeutic efficiency of chemotherapy or immuno-therapy, including cell therapy or appropriate combinations of therapeutics. The role of effector immune cells in the development and progression of DLBCL is complex and involves reciprocal interactions between tumor cells, adaptive and innate immune cells, their soluble mediators, and structural components present in the TME. Recruitment of immune cells in the TME and their distinct effects on tumor progression and therapeutic outcomes in the presence of therapy have decisive effects on the outcome of therapy. In this review, we discuss the application and implications of binary therapy involving suboptimal-dose chemotherapy and adoptive cell therapy on the basis of our recent findings on γc cytokine-aided cross-talk between dendritic cells and natural killer cells in therapy against experimental murine lymphoma. This novel therapeutic protocol induces a healing response in experimental lymphoma by downregulating FOXP3 and programmed cell death protein 1. We discuss the various aspects of binary therapy covering multiple issues, including the participation of cell subsets and checkpoint inhibitors in the treatment of malignant lymphoma. These new therapies involve the induction of adoptive cell therapy through the passive transfer of immunologic effectors in addition to a suboptimal dose of adriamycin (doxorubicin hydrochloride) to increase the ability of the immune system to react against tumor antigens, inducing the destruction of tumor cells.