Clinical & Developmental Immunology最新文献

{"title":"Systemic Autoimmune Diseases","authors":"Guixiu Shi, Jianying Zhang, Zhixin Zhang, Xuan Zhang","doi":"10.1155/2013/728574","DOIUrl":"https://doi.org/10.1155/2013/728574","url":null,"abstract":"Systemic autoimmune diseases are a broad range of related diseases characterized by dysregulation of immune system which give rise to activation of immune cells to attack autoantigens and resulted in inappropriate inflammation and multitissue damages. They are a fascinating but poorly understood group of diseases, ranging from the commonly seen rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE) to the relatively rare systemic sclerosis [1]. The mechanism of pathogenesis of systemic autoimmune diseases is still not very clear. It is now considered that genetic factors, infection, endocrine, and environmental exposure are involved in the pathogenesis of these diseases [2–4]. There is no treatment strategy to cure this kind of disease at present which gives rise to the needs of long-term lasting treatment, making systemic autoimmune diseases be a mounting public health concern for the foreseeable future. Vital organs such as lung and kidney involvement in systemic autoimmune diseases are common and always presented in a progressive pattern with limited treatment strategy, making them be one of the most common causes of death in patients [5]. \u0000 \u0000Based on this background, we assembled this special issue for a better understanding of systemic autoimmune diseases, on aspects of mechanisms of pathogenesis, diagnosis, and treatment, including papers ranging from the basic researches to clinical researches and reviews about systemic autoimmune diseases. \u0000 \u0000Studies on the basic research of systemic autoimmune disease in this issue provided us new insights into the mechanism of the pathogenesis of systemic autoimmune disease. The role of HMGB1 in the T-cell DNA demethylation was discussed in the paper of Y. Li et al. SNPs with strong RA association signal in the British were analyzed in Han Chinese by H. Li et al., and the methylation status of miR-124a loci in synovial tissues of RA patients was analyzed by Q. Zhou et al. indicating the epigenetic factor in the pathogenesis of RA. Expression of microRNA-155 was studied by L. Long et al. in RA patients. IL-33 status was tested in RA patients by S. Tang et al. D. Lorton et al. and Y. Du et al. indicated the possible role of beta2-adrenergic receptors (β2-AR) and p53 apoptosis effector related to PMP-22(Perp) in the pathogenesis of RA, respectively. It has long been demonstrated that γδ T cells play important roles in the development of autoimmune diseases; the precise role of γδ T cells in the pathogenesis of SLE was studied by Z. Lu et al. Z. Gu et al. discussed the role of p53/p21 pathway in the pathogenesis of SLE. X. Gan et al. demonstrated the role of GITR and GITRL in the primary Sjogren's syndrome. The expression of IL-6 and its clinical significance in patients with dermatomyositis was discussed by M. Yang et al. L. Estrada-Capetillo et al. found that DCs from patients with rheumatic inflammatory disease show an aberrant function that may have an important role in the pathogenesis. S. St","PeriodicalId":55254,"journal":{"name":"Clinical & Developmental Immunology","volume":"2013 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2013-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2013/728574","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"64227517","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Crosstalk between the Bone and the Immune System: Osteoimmunology","authors":"G. Brunetti, G. Mori, P. D’Amelio, R. Faccio","doi":"10.1155/2013/617319","DOIUrl":"https://doi.org/10.1155/2013/617319","url":null,"abstract":"Osteoimmunology is an interdisciplinary research field focused on the molecular understanding of the interplay between the skeletal and immune systems. Recent reports suggest that a large number of molecules affect both bone and immune cells. Furthermore, it has been demonstrated that immune cells express molecules modulating bone cell development and bone is known to provide important signal to the hematopoietic and immune cells, which develop in the bone marrow and then migrate to peripheral organs. \u0000 \u0000All these concepts are well represented in this special issue, starting from a large overview of bone cell differentiation, followed by the general mechanisms highlighting the interaction between bone and immune cells described by G. Mori et al. The effect of the numerous T-cell subsets on bone cells is very complex. In particular, a clear overview on Th17 and Treg and their involvement in bone diseases is presented by M. Wang et al., whereas a more detailed description of the negative regulatory feedback loop between osteoclasts and CD8+ T cells that contributes to homeostasis of both the skeletal and immune systems is provided by Z. S. Buchwald and R. Aurora. \u0000 \u0000The first identified pioneer cytokine regulating both bone and immune systems is RANKL, revised by N. Lo Iacono et al. The authors also report that a genetic defect impairing RANKL function leads to a peculiar form of an invalidating rare bone disease, named autosomal recessive osteopetrosis. In addition to RANKL, TNF-alpha is another cytokine known to play a fundamental role during osteoclastogenesis in the context of inflammatory arthritis, as described by H. Kitaura et al. Comprehensive reports detailing the interaction between bone and immune cells in the periodontal diseases and postmenopausal osteoporosis are reported, respectively, by A. Di Benedetto et al. and M. F. Faienza et al. The involvement of T cells in bone metastatic solid tumors has been carefully reviewed by I. Roato. Immune cell contribution in multiple myeloma bone disease is well described by A. Oranger et al. Understanding how bone and immune cells mutually interact with each other can give rise to new therapeutical targets as described by A. Corrado et al. in the context of rheumatoid arthritis. Moreover, T. Fujimura et al. demonstrated that, in invasive extramammary Paget's disease, the administration of bisphosphonates, privileged antiresorptive drugs, has also an immunosuppressive role in addition to blocking osteoclast activity. \u0000 \u0000Recent findings suggested that immune cells are critical mediators of the effect of different hormones on bone cells. In particular, G. Colaianni et al. analyzed the Pituitary/Immune/Bone Axis, highlighting the effect immune cell-mediated of hormones such as FSH and TSH on bone remodeling. Finally, further sustaining the role of bone cells on the regulation of haematopoiesis, C. L. Sesler and M. Zayzafoon demonstrated that the inhibition of NFAT activation in osteoblasts increases ","PeriodicalId":55254,"journal":{"name":"Clinical & Developmental Immunology","volume":"2013 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2013-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2013/617319","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"64180400","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Immunobiology and Pharmacologic Manipulation of Dendritic and Regulatory Cells","authors":"M. Mohty, A. Nagler, N. Kröger, B. Gaugler","doi":"10.1155/2013/186983","DOIUrl":"https://doi.org/10.1155/2013/186983","url":null,"abstract":"Antigen presenting cells (APCs), especially dendritic cells (DCs), play a major role in the hierarchy of the induction of immune reactions. DCs are widely accepted as the most potent APCs capable of inducing protective adaptive immune responses in addition to tolerance to self-antigens. The role of DCs is currently being investigated in the context of many disease and therapeutic settings. In response to a variety of microbial and endogenous stimuli, resting DCs in peripheral tissues undergo a complex maturation process that might involve the regulation of genes that control distinct DC functions. The different functional properties of DCs are also linked to the existence of several subpopulations in humans and animals that differ in response to stimuli. In this special issue, several articles addressed some recent findings highlighting the interactions between key immune effectors both in vitro and in vivo and in different disease settings. \u0000 \u0000V. R. Yanofsky et al. provided an in-depth analysis of DC biology, with a particular focus on skin DCs and their role in cutaneous carcinoma. C. Y. J. Chung et al. provided an overview of the role of DCs in the immunopathogenesis of autoimmunity, as well as recent concepts of DC-based therapeutic opportunities in autoimmune diseases. On the other hand, P. Ruiz et al. described the different treatments and some of the novel immunotherapeutic strategies undertaken to induce transplantation tolerance in general. More specifically, M. Michael et al. discussed the current knowledge of Treg biology and its potential for cell-based immunotherapy in allogeneic stem cell transplantation. The review by A. K. Gloudemans et al. summarized the latest literature on the role of mucosal IgA in protection against allergic airway disease, the mechanisms described to induce secretory IgA, and the role of (mucosal) DCs in this process. \u0000 \u0000D.-Y. Chen et al. examined the effect of dextromethorphan (DXM), a common cough suppressant, on the activation and function of DCs. Interestingly, DXM decreased the LPS-induced surface expression of CD80, CD83, and HLA-DR and the secretion of IL-6 and IL-12 in human monocyte-derived DCs. These findings provide a new insight into the impact of DXM treatment on DCs and suggest that DXM has the potential to be used in treating DC-related acute and chronic diseases. Similarly, L. Adalid-Peralta et al. showed that cysticerci may modulate DCs to favor a suppressive environment, which may help parasite establishment, minimizing the excessive inflammation, which may lead to tissue damage. In the same line, R. N. Ramos et al. described that cytokines such as IL-10 and TGF-beta, as well as cell surface molecules like PD-L1 and ICOS, seem to be significantly involved in the redirection of DCs towards tolerance induction, and tumor cells may modulate distinct DC subpopulations through the involvement of these molecules. Another work from X. Gu et al. suggested that regulation of B7-H1 expression on hepa","PeriodicalId":55254,"journal":{"name":"Clinical & Developmental Immunology","volume":"2013 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2013-06-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2013/186983","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"64388431","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Alloreactivity-Based Medical Conditions","authors":"S. Vukmanović, M. Petroff, A. Stevens, D. Rukavina","doi":"10.1155/2013/567084","DOIUrl":"https://doi.org/10.1155/2013/567084","url":null,"abstract":"Alloreactivity is a response of the immune system to individual antigenic differences within species. These responses in general occur following exposure to alloantigens as a consequence of medical intervention (such as transfusion or tissue transplantation) or during pregnancy. Responses to alloantigens form a basis of a broad spectrum of medical conditions, such as graft rejection, graft versus host disease, reaction to blood (products), or biopharmaceuticals and fetal and neonatal diseases (thrombocytopenia, hemolytic anemia, hemochromatosis, biliary atresia, and glomerulopathy). On the other hand, normal pregnancies are often accompanied by strongly tolerogenic responses to fetal alloantigens. Diverse immunologic components, including T cells, antibodies (B cells), and NK cells, promote alloreactivity, and this complexity makes the pathogenesis and tolerogenesis of these conditions distinct and unique. This special issue contains seven manuscripts touching on various aspects of alloreactivity in medicine. \u0000 \u0000Blocking CD40-CD40L interaction can induce acceptance of cardiac allografts. However, the blockade is less efficient under inflammatory conditions. In “Glucocorticoid-induced TNFR-related protein reverses cardiac allograft acceptance induced by CD40-CD40L blockade,” Krill et al. demonstrate that stimulation of GITR (a cell surface molecule displayed by effector and regulatory T cells) can initiate cardiac graft rejection irrespective of the presence or absence of CD40-CD40L blockade, defining thus at least one possible molecular mechanism of resistance to CD40-CD40L suppression. The balance between the effector and regulatory T cells is critical for development of graft-specific immune responses in general. Franzese et al. review the usefulness of this balance in predicting or establishing the diagnosis of graft rejection in “Regulatory T cells in the immunodiagnosis and outcome of kidney allograft rejection.” \u0000 \u0000Allogeneic hematopoietic stem cell transplantation is used for treatment of autoimmune diseases, multiple organ transplantation, consequences of supralethal irradiation and advanced malignancies and other serious conditions refractory to conventional methods. In “New allogeneic hematopoietic cell transplantation method: hematopoietic cell transplantation plus thymus transplantation for intractable diseases,” Hosaka demonstrates that allogeneic hematopoietic stem cell transplantation combined with the same donor thymus transplantation has a superior effect producing more efficient T cell function and reduced graft versus host disease. \u0000 \u0000Redzovic et al., in “Mucins help to avoid alloreactivity at the maternal fetal interface,” review roles of mucin-1 and tumor associated glycoprotein-72 in regulating immune responses. Parallels are drawn between the ability of these molecules to promote tumor growth, invasion, and metastasis and to prevent trophoblast invasion. Removing glycoproteins TAG-72 and Muc 1 from the eutopic implantation ","PeriodicalId":55254,"journal":{"name":"Clinical & Developmental Immunology","volume":"2013 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2013-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2013/567084","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"64156722","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Role of microglia in CNS autoimmunity.","authors":"Tobias Goldmann,&nbsp;Marco Prinz","doi":"10.1155/2013/208093","DOIUrl":"https://doi.org/10.1155/2013/208093","url":null,"abstract":"<p><p>Multiple sclerosis (MS) is the most common autoimmune disease of the central nervous system (CNS) in the Western world. The disease is characterized histologically by the infiltration of encephalitogenic TH1/TH17-polarized CD4(+) T cells, B cells, and a plethora of myeloid cells, resulting in severe demyelination ultimately leading to a degeneration of neuronal structures. These pathological processes are substantially modulated by microglia, the resident immune competent cells of the CNS. In this overview, we summarize the current knowledge regarding the highly diverse and complex function of microglia during CNS autoimmunity in either promoting tissue injury or tissue repair. Hence, understanding microglia involvement in MS offers new exciting paths for therapeutic intervention. </p>","PeriodicalId":55254,"journal":{"name":"Clinical & Developmental Immunology","volume":"2013 ","pages":"208093"},"PeriodicalIF":0.0,"publicationDate":"2013-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2013/208093","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31212194","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Role of bacterial lipopolysaccharide in enhancing host immune response to Candida albicans.","authors":"Helen Rogers,&nbsp;David W Williams,&nbsp;Gui-Jie Feng,&nbsp;Michael A O Lewis,&nbsp;Xiao-Qing Wei","doi":"10.1155/2013/320168","DOIUrl":"https://doi.org/10.1155/2013/320168","url":null,"abstract":"<p><p>Human infections involving yeast of the genus Candida often occur in the presence of bacteria, and, as such, it is important to understand how these bacteria influence innate host immunity towards Candida. Dectin-1 is a cell receptor of macrophages for Candida albicans recognition. The aim of this study was to examine dectin-1 expression by monocytes after stimulation with bacterial lipopolysaccharide (LPS), followed by heat-killed C. albicans (HKC). Freshly isolated human peripheral blood monocytes (PBMCs) and human monocytes cell line (THP-1) cells expressed low levels of dectin-1. Stimulation with LPS and GM-CSF/IL-4 was found to increase dectin-1 expression in both CD14(+) human PBMC and THP-1 cells. Enhanced dectin-1 expression resulted in increased phagocytosis of Candida. When THP-1 cells were challenged only with HKC, detectable levels of IL-23 were not evident. However, challenge by LPS followed by varying concentrations of HKC resulted in increased IL-23 expression by THP-1 cells in HKC dose-dependent manner. Increased expression of IL-17 by PBMC also occurred after stimulation with Candida and LPS. In conclusion, bacterial LPS induces an enhanced immune response to Candida by immune cells, and this occurs through increasing dectin-1 expression.</p>","PeriodicalId":55254,"journal":{"name":"Clinical & Developmental Immunology","volume":"2013 ","pages":"320168"},"PeriodicalIF":0.0,"publicationDate":"2013-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2013/320168","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31232410","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neonatal sepsis due to coagulase-negative staphylococci.","authors":"Elizabeth A Marchant,&nbsp;Guilaine K Boyce,&nbsp;Manish Sadarangani,&nbsp;Pascal M Lavoie","doi":"10.1155/2013/586076","DOIUrl":"https://doi.org/10.1155/2013/586076","url":null,"abstract":"<p><p>Neonates, especially those born prematurely, are at high risk of morbidity and mortality from sepsis. Multiple factors, including prematurity, invasive life-saving medical interventions, and immaturity of the innate immune system, put these infants at greater risk of developing infection. Although advanced neonatal care enables us to save even the most preterm neonates, the very interventions sustaining those who are hospitalized concurrently expose them to serious infections due to common nosocomial pathogens, particularly coagulase-negative staphylococci bacteria (CoNS). Moreover, the health burden from infection in these infants remains unacceptably high despite continuing efforts. In this paper, we review the epidemiology, immunological risk factors, diagnosis, prevention, treatment, and outcomes of neonatal infection due to the predominant neonatal pathogen CoNS.</p>","PeriodicalId":55254,"journal":{"name":"Clinical & Developmental Immunology","volume":"2013 ","pages":"586076"},"PeriodicalIF":0.0,"publicationDate":"2013-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2013/586076","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31502456","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Immunological reaction in TNF-α-mediated osteoclast formation and bone resorption in vitro and in vivo.","authors":"Hideki Kitaura,&nbsp;Keisuke Kimura,&nbsp;Masahiko Ishida,&nbsp;Haruka Kohara,&nbsp;Masako Yoshimatsu,&nbsp;Teruko Takano-Yamamoto","doi":"10.1155/2013/181849","DOIUrl":"https://doi.org/10.1155/2013/181849","url":null,"abstract":"<p><p>Tumor necrosis factor- α (TNF- α ) is a cytokine produced by monocytes, macrophages, and T cells and is induced by pathogens, endotoxins, or related substances. TNF- α may play a key role in bone metabolism and is important in inflammatory bone diseases such as rheumatoid arthritis. Cells directly involved in osteoclastogenesis include macrophages, which are osteoclast precursor cells, osteoblasts, or stromal cells. These cells express receptor activator of NF- κ B ligand (RANKL) to induce osteoclastogenesis, and T cells, which secrete RANKL, promote osteoclastogenesis during inflammation. Elucidating the detailed effects of TNF- α on bone metabolism may enable the identification of therapeutic targets that can efficiently suppress bone destruction in inflammatory bone diseases. TNF- α is considered to act by directly increasing RANK expression in macrophages and by increasing RANKL in stromal cells. Inflammatory cytokines such as interleukin- (IL-) 12, IL-18, and interferon- γ (IFN- γ ) strongly inhibit osteoclast formation. IL-12, IL-18, and IFN- γ induce apoptosis in bone marrow cells treated with TNF- α   in vitro, and osteoclastogenesis is inhibited by the interactions of TNF- α -induced Fas and Fas ligand induced by IL-12, IL-18, and IFN- γ . This review describes and discusses the role of cells concerned with osteoclast formation and immunological reactions in TNF- α -mediated osteoclastogenesis in vitro and in vivo.</p>","PeriodicalId":55254,"journal":{"name":"Clinical & Developmental Immunology","volume":"2013 ","pages":"181849"},"PeriodicalIF":0.0,"publicationDate":"2013-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2013/181849","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31503018","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"What are the molecules involved in regulatory T-cells induction by dendritic cells in cancer?","authors":"Rodrigo Nalio Ramos,&nbsp;Cristiano Jacob de Moraes,&nbsp;Bruna Zelante,&nbsp;José Alexandre M Barbuto","doi":"10.1155/2013/806025","DOIUrl":"https://doi.org/10.1155/2013/806025","url":null,"abstract":"<p><p>Dendritic cells (DCs) are essential for the maintenance of homeostasis in the organism, and they do that by modulating lymphocyte priming, expansion, and response patterns according to signals they receive from the environment. The induction of suppressive lymphocytes by DCs is essential to hinder the development of autoimmune diseases but can be reverted against homeostasis when in the context of neoplasia. In this setting, the induction of suppressive or regulatory T cells contributes to the establishment of a state of tolerance towards the tumor, allowing it to grow unchecked by an otherwise functional immune system. Besides affecting its local environment, tumor also has been described as potent sources of anti-inflammatory/suppressive factors, which may act systemically, generating defects in the differentiation and maturation of immune cells, far beyond the immediate vicinity of the tumor mass. Cytokines, as IL-10 and TGF-beta, as well as cell surface molecules like PD-L1 and ICOS seem to be significantly involved in the redirection of DCs towards tolerance induction, and recent data suggest that tumor cells may, indeed, modulate distinct DCs subpopulations through the involvement of these molecules. It is to be expected that the identification of such molecules should provide molecular targets for more effective immunotherapeutic approaches to cancer.</p>","PeriodicalId":55254,"journal":{"name":"Clinical & Developmental Immunology","volume":"2013 ","pages":"806025"},"PeriodicalIF":0.0,"publicationDate":"2013-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2013/806025","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31503384","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"New insights on human polyomavirus JC and pathogenesis of progressive multifocal leukoencephalopathy.","authors":"Anna Bellizzi,&nbsp;Elena Anzivino,&nbsp;Donatella Maria Rodio,&nbsp;Anna Teresa Palamara,&nbsp;Lucia Nencioni,&nbsp;Valeria Pietropaolo","doi":"10.1155/2013/839719","DOIUrl":"https://doi.org/10.1155/2013/839719","url":null,"abstract":"<p><p>John Cunningham virus (JCV) is a member of the Polyomaviridae family. It was first isolated from the brain of a patient with Hodgkin disease in 1971, and since then the etiological agent of the progressive multifocal leukoencephalopathy (PML) was considered. Until the human immunodeficiency virus (HIV) pandemic, PML was rare: in fact HIV-induced immunodeficiency is the most common predisposing factor accounting for 85% of all instances of PML. This data led to intense research on JCV infection and resulted in better understanding of epidemiology and clinic-pathologic spectrum. Recently, cases of PML have been observed after the introduction of monoclonal antibodies, such as natalizumab, rituximab, efalizumab, and infliximab, in the treatment of autoimmune disease, underlining the important role of host immunity in PML pathogenesis. In this review current understanding of the JCV infection and the new findings relating to the pathogenesis of PML has been comprehensively revised, focusing our attention on the interaction between the cellular and viral molecular pathways implicated in the JCV infection and the modulating role of host immune surveillance in the viral reactivation from a latent state.</p>","PeriodicalId":55254,"journal":{"name":"Clinical & Developmental Immunology","volume":"2013 ","pages":"839719"},"PeriodicalIF":0.0,"publicationDate":"2013-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2013/839719","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31538063","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}