International immunology最新文献

{"title":"Salmonella Typhimurium evades from host immunity and antibiotics in monocytes.","authors":"Uki Kimura, Nobuhiro Matsuyama, Karen Saiki, Sei Kashima, Hiroki Takahashi, Akiko Takaya, Koji Tokoyoda","doi":"10.1093/intimm/dxaf077","DOIUrl":"10.1093/intimm/dxaf077","url":null,"abstract":"<p><p>Intracellular bacteria can survive in vivo, evading host immunity and antibiotics. Salmonella persists in organs such as the spleen by invading the phagocytic cells. However, it remains controversial which specific cell populations, e.g. macrophages, monocytes, neutrophils, or dendritic cells, harbor the bacteria during persistent infection. To address this question, we employed a persistent infection mouse model using attenuated Salmonella expressing an acid tolerant fluorescent protein. We found that the bacteria predominantly resided in monocytes. Although these cells expressed Ly-6G, a typical marker for neutrophils, they did not exhibit a polymorphonuclear morphology. Furthermore, Salmonella primarily and preferentially invaded monocytes over other phagocytic cell types. Importantly, Salmonella was able to survive in monocytes even in the presence of antibiotics. Our findings demonstrate that monocytes serve as a critical survival niche for Salmonella in vivo, allowing the bacteria to evade both host immunity and antibiotics.</p>","PeriodicalId":13743,"journal":{"name":"International immunology","volume":" ","pages":"335-343"},"PeriodicalIF":3.2,"publicationDate":"2026-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145804280","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Zika virus exacerbates encephalomyelitis by inducing the production of T cell-attracting chemokines in astrocytes.","authors":"Naganori Kamiyama, Benjawan Saechue, Nozomi Sachi, Thanyakorn Chalalai, Astri Dewayani, Masaaki Okamoto, Sotaro Ozaka, Yasuhiro Soga, Yomei Kagoshima, Supanuch Ekronarongchai, Shinya Hidano, Makoto Tsuda, Takashi Kobayashi","doi":"10.1093/intimm/dxaf075","DOIUrl":"10.1093/intimm/dxaf075","url":null,"abstract":"<p><p>Recent outbreaks of the ZIKA virus (ZIKV) in Brazil and Puerto Rico have been linked to an increase in the incidence of fetal microcephaly and Guillain-Barré syndrome. In addition, although a causal relationship remains unproven, ZIKV has been found in the brains of multiple sclerosis (MS) patients, prompting interest in a possible link. The present study aimed to elucidate the role of ZIKV in the pathogenesis of MS. ZIKV-infected mice with experimental autoimmune encephalomyelitis (EAE) exhibited aggravated EAE symptoms with significant demyelination of the central nervous system (CNS). Moreover, ZIKV infection promoted pathogenic T cell infiltration into the CNS by enhancing the expression of chemokines for C-C motif chemokine receptor 2 (CCR2) in astrocytes, which was dependent on tumor necrosis factor receptor-associated factor 6 (TRAF6) signaling. Propagermanium, a CCR2 inhibitor, prevented ZIKV-induced exacerbation of EAE in mice. These findings highlight the critical role of TRAF6 signaling in the progression of neurological disorders caused by ZIKV infection.</p>","PeriodicalId":13743,"journal":{"name":"International immunology","volume":" ","pages":"318-334"},"PeriodicalIF":3.2,"publicationDate":"2026-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13150445/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145767896","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"TLR7 responses to nucleosides drive sialadenitis in Slc29a3-deficient mice.","authors":"Takuma Shibata, Kotono Okabe-Kibe, Hu Chen, Kiyoshi Yamaguchi, Daisuke Koga, Masato Taoka, Yuji Motoi, Ryota Sato, Hao-Wen Hsiao, Ryutaro Fukui, Naoki Kaneko, Zhiqin Wang, Yanmei Li, Wei Wei, Zhigang Cai, Yoichi Furukawa, Emi K Nishimura, Shintaro Kawano, Masafumi Moriyama, Seiji Nakamura, Kensuke Miyake","doi":"10.1093/intimm/dxaf073","DOIUrl":"10.1093/intimm/dxaf073","url":null,"abstract":"<p><p>Autoimmune sialadenitis is a hallmark of IgG4-related disease (IgG4-RD) and Sjögren syndrome. The single-stranded RNA sensor TLR7 has been shown as a driver of sialadenitis. Although TLR7 is activated by ssRNA degradation products such as nucleosides and oligoribonucleotides, the role of these ligands in sialadenitis development remains unclear. Here, we demonstrate that lysosomal accumulation of endogenous nucleosides is sufficient to drive autoimmune sialadenitis. Loss-of-function genetic variations in the nucleoside transporter SLC29A3 cause lysosomal nucleoside accumulation, leading to constitutive activation of TLR7 and TLR8 in monocytes and macrophages. Consequently, macrophages infiltrate multiple organs in mice and humans. In Slc29a3-/- mice, submandibular glands (SMGs) were impaired in saliva production. SLC29A3-deficiency specifically damaged Aqp5+ acinar and intercalated duct cells in SMGs, while sparing neighboring cells such as ductal and myoepithelial cells. Although macrophages accumulated in both the spleen and SMGs, lymphocyte infiltration and production of chemokines, including CXCL9, CXCL13, and CCL5, occurred selectively in SMGs. In IgG4-RD patients, these chemokines were also produced in SMGs, highlighting parallels between sialadenitis in Slc29a3-/- mice and IgG4-RD. These findings indicate that constitutive TLR7 activation by nucleosides is a key mechanism driving autoimmune sialadenitis.</p>","PeriodicalId":13743,"journal":{"name":"International immunology","volume":" ","pages":"306-317"},"PeriodicalIF":3.2,"publicationDate":"2026-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145661058","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Selective decreases in regulatory B cell (Breg) subsets in active uveitis: IL-10+CD19+CD24hiCD38hiBreg in patients and B10 Breg in mice.","authors":"Yi-Hsing Chen, Xiaozhe Zhang, Malihe Eskandarpour, Rose M Gilbert, Sue Lightman, Virginia L Calder","doi":"10.1093/intimm/dxag021","DOIUrl":"https://doi.org/10.1093/intimm/dxag021","url":null,"abstract":"<p><p>Several regulatory B lymphocyte (Breg) subsets have been implicated in autoimmune diseases. We investigated Breg subsets in non-infectious uveitis (NIU) and in mouse models of experimental autoimmune uveitis (EAU). Bloods from NIU patients with active disease (n=13), in remission (n=37) and healthy controls (n=10) were immunophenotyped for CD19+CD24hiCD38lo, CD19+CD24hiCD38hi immature (iBreg) and CD19+CD38intCD24int-mature Breg. In NIU, levels of peripheral blood iBreg and serum IL-10 were decreased in active disease vs. remission (P<0.01). In quiescent NIU, iBreg were isolated and, when added at increasing ratios to autologous CD3+T cells, downregulated T cell proliferation. In an EAU model, at peak disease, CD19+CD1dhiCD5+-B10, CD19+CD5+-B1, transitional 2 marginal-zone precursor CD19+CD21hiCD24hiCD23+-T2-MZP and marginal-zone B CD19+CD21hiCD23--MZB Breg subsets were analyzed both phenotypically and functionally. In EAU spleens, all Breg subsets investigated were detectable, but the IL-10-expressing B10 Breg subset was immunosuppressive and inversely correlated with disease severity (P = 0.048, R2 = 0.47). Blood-derived IL-10-expressing B10 and B1 Breg cells were increased in both adjuvant controls and EAU but were significantly reduced in clinically milder EAU. In dissociated retinal cells, only the B10 Breg subset was detectable and increased in EAU. Selective Breg subsets may be immunosuppressive, with iBreg in NIU and IL-10-expressing B10 Bregs in EAU.</p>","PeriodicalId":13743,"journal":{"name":"International immunology","volume":" ","pages":""},"PeriodicalIF":3.2,"publicationDate":"2026-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147837609","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Generation of CD68+ macrophage-depleted NOG mice for in vivo engraftment of human red blood cells.","authors":"Yusuke Ohno, Misa Mochizuki, Kenji Kawai, Motohito Goto, Riichi Takahashi, Ryoji Ito","doi":"10.1093/intimm/dxaf072","DOIUrl":"10.1093/intimm/dxaf072","url":null,"abstract":"<p><p>Humanized mice are invaluable models for investigating human cell engraftment in vivo post-transplantation. Mice engrafted with human red blood cells (hRBCs) are useful for examining the physiological roles of hRBCs in vivo, including studies on blood disorders, immune responses, and transfusion-related research. These models hold promise for malaria infection studies and vaccine development. However, engrafted hRBCs in vivo in immunodeficient mice present challenges that must be addressed to establish effective in vivo models. In this study, we explored the rejection mechanisms of hRBCs in immunodeficient NOD/Shi-scid-IL2rγnull (NOG) mice and developed a novel model for long-term RBC engraftment. We observed rapid depletion of fluorescently labeled hRBCs in the liver, but not in other organs, of NOG mice, with Gr-1midCD68+ mouse macrophages playing a significant role in the elimination of hRBCs in the liver. To counteract this, we created thymidine kinase (TK) transgenic (Tg) mice under the human CD68 promoter (NOG-pCD68-TK Tg), which, upon administration of valganciclovir (VGCV), led to the successful depletion of macrophages. Consequently, hRBCs showed significantly prolonged engraftment in NOG-pCD68-TK Tg mice compared to non-Tg mice following macrophage depletion, maintaining engraftment for up to 14 d post-transplantation. This study elucidates the erythrophagocytosis mechanisms of hRBCs in mice and establishes NOG-pCD68-TK Tg mice as a valuable model for the long-term engraftment of hRBCs, potentially advancing in vivo hRBC research.</p>","PeriodicalId":13743,"journal":{"name":"International immunology","volume":" ","pages":"296-305"},"PeriodicalIF":3.2,"publicationDate":"2026-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145661039","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Microbiota regulation of gut-brain neuroimmune crosstalk in early life.","authors":"Purnima Ravisankar, Daniel S H Wong, Melody Y Zeng","doi":"10.1093/intimm/dxaf076","DOIUrl":"10.1093/intimm/dxaf076","url":null,"abstract":"<p><p>In early life, the immune and nervous systems are highly plastic and engage in complex, bidirectional communication that is critical for establishing postnatal immune tolerance, gut and brain development, and responses to environmental challenges. The developing gut microbiota exerts its influence on both systems via microbial metabolites to modulate immune responses and neural function. Early disruptions in the gut microbiota, in part because of preterm delivery or antibiotic treatment, are linked to long-term immune or neurodevelopmental impairments. In this review, we provide an overview of the current understanding of how the microbiota crosstalk with immune cells regulates the development and function of the nervous system.</p>","PeriodicalId":13743,"journal":{"name":"International immunology","volume":" ","pages":"282-295"},"PeriodicalIF":3.2,"publicationDate":"2026-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145780749","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Distinct fibrosis-associated macrophage subsets coordinate iron metabolism in pulmonary fibrosis.","authors":"Hiroshi Nabeshima, Kiyoharu Fukushima, Yu-Chen Liu, Daisuke Motooka, Takayuki Niitsu, Eriko Fukui, Michiko Ichii, Takuro Nii, Yuri Akamine, Nanako Hamada, Kazuki Hashimoto, Yuko Abe, Yasuharu Nagahama, Takanori Matsuki, Kazuyuki Tsujino, Keisuke Miki, James Badger Wing, Naoki Hosen, Yasushi Shintani, Atsushi Kumanogoh, Daisuke Okuzaki, Hiroshi Kida, Shizuo Akira","doi":"10.1093/intimm/dxag017","DOIUrl":"https://doi.org/10.1093/intimm/dxag017","url":null,"abstract":"<p><p>Pulmonary fibrosis has a poor prognosis due to challenges in early diagnosis and therapeutic intervention. Current treatments remain largely ineffective due to an incomplete understanding of the complex pathology, including the interactions between fibroblasts and profibrotic immune cells within fibrotic lungs. To elucidate the dynamics of fibrosis, we performed single-cell RNA sequencing (scRNA-seq) on bronchoalveolar lavage fluid (BALF) obtained from patients with interstitial lung disease (ILD). We identified the SPP1- and APOE-expressing macrophage population that is commonly present across ILDs. Histological analysis showed that this macrophage population accumulated at the center of fibrotic foci. Furthermore, the ratio of this macrophage population was increased in both progressive pulmonary fibrosis (PPF) and idiopathic pulmonary fibrosis (IPF). Transcriptomic analysis further divided this macrophage population into two subsets: SLC40A1+ or HAMP+ fibrosis-associated macrophages. We found that the relative balance of IL-10 and IL-8 regulated SLC40A1 and HAMP expression within fibrosis-associated macrophages. Additionally, histological analysis revealed that bronchial epithelium expressed IL-8, while type II alveolar epithelial cells expressed IL-10 in the fibrotic lung. SLC40A1+ fibrosis-associated macrophages localized to CD31+ perivascular regions and mediated the uptake and degradation of the hemoglobin-haptoglobin complex. This dual pathway-providing iron via SLC40A1 and intracellular iron accumulation via HAMP-facilitated the transition of fibroblasts into SPP1+ myofibroblasts. Moreover, ferroptotic fibroblasts secreted TGF-β1, which further contributes to fibrotic progression. In conclusion, aberrant iron metabolism orchestrated by fibrosis-associated macrophages may contribute to fibrosis by facilitating the transition of myofibroblasts. These findings provide mechanistic insight into the progression of autonomous pulmonary fibrosis.</p>","PeriodicalId":13743,"journal":{"name":"International immunology","volume":" ","pages":""},"PeriodicalIF":3.2,"publicationDate":"2026-04-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147770665","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"PDLIM4 promotes dephosphorylation of STAT transcription factors by recruiting PTP-BL and inhibits Th1, Th2, and Th17 cell differentiation.","authors":"Aya Jodo, Masakiyo Nakahira, Yuta Kochi, Akiko Sugimoto-Ishige, Tsuneyasu Kaisho, Takashi Tanaka","doi":"10.1093/intimm/dxag019","DOIUrl":"https://doi.org/10.1093/intimm/dxag019","url":null,"abstract":"<p><p>STAT transcription factors are activated by tyrosine phosphorylation after cytokine stimulation and are critical for the differentiation of T-helper (Th) cells into particular Th lineage subsets. How STAT-mediated Th cell differentiation is negatively regulated, however, is not fully understood. Here, we report that PDLIM4 binds to STAT3, 4, and 6 and suppresses gene activation mediated by these STATs. PDLIM4 acts as an adaptor that recruits PTP-BL, a protein tyrosine phosphatase, through its LIM domain, facilitating dephosphorylation of STAT proteins. PDLIM4-deficiency in CD4+ T cells resulted in augmented tyrosine phosphorylation of these STAT proteins and consequently enhanced Th1, Th2 and Th17 cell differentiation, suggesting that PDLIM4 regulates the differentiation of multiple lineages of Th cells by suppressing STAT signaling. We further found that a non-synonymous single-nucleotide polymorphism (nsSNP) in PDLIM4, which causes the substitution of a glycine residue with a cysteine in the LIM domain, is associated with susceptibility to rheumatoid arthritis and Graves' disease, both of which are known to be Th17 cell-driven autoimmune diseases. Notably, PDLIM4 containing this amino acid substitution in the LIM domain showed reduced binding to PTP-BL and was therefore partially impaired in its ability to dephosphorylate STAT3 and suppress STAT3 signaling. Our findings define an essential role of PDLIM4 in negatively regulating STAT-mediated T helper cell differentiation and preventing the onset of human autoimmune diseases.</p>","PeriodicalId":13743,"journal":{"name":"International immunology","volume":" ","pages":""},"PeriodicalIF":3.2,"publicationDate":"2026-04-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147770681","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Lipid metabolic regulation of pathogenic type 2 immunity in the airway.","authors":"Hiroyuki Yagyu, Masahiro Kiuchi, Kiyoshi Hirahara","doi":"10.1093/intimm/dxag015","DOIUrl":"https://doi.org/10.1093/intimm/dxag015","url":null,"abstract":"<p><p>Immune memory is central to host protection against pathogens and contributes to the pathogenesis of chronic inflammatory diseases. Beyond canonical cytokines and antigenic stimuli, metabolic signals have emerged as pivotal regulators of T-cell activation, differentiation, and memory formation. However, the mechanisms by which metabolic and tissue-derived cues imprint pathogenic features on T cells remain poorly understood. Dysregulation of type 2 immune memory is a major driver of chronic inflammation in allergic diseases. A distinct subpopulation of memory T helper 2 (Th2) cells that express the interleukin (IL)-33 receptor ST2 has emerged as a key contributor to the pathogenesis of chronic allergic inflammation. Recent studies have revealed a close link between lipid metabolism and pathogenic type 2 immunity, highlighting how fatty acid uptake, storage within lipid droplets, and catabolism through lipolysis and lipophagy regulate the expression of ST2 and cytokine production. Moreover, transcriptional regulators such as peroxisome proliferator-activated receptor γ (PPARγ) integrate lipid-derived signals with transcriptional and metabolic programs that induce pathogenic memory. In this review, we summarize the current understanding of CD4+ T cell-mediated immune memory, with a particular focus on pathogenic Th2 cells and airway type 2 immunity, and discuss emerging concepts that connect lipid metabolic programs, transcriptional regulation, and chronic allergic inflammation.</p>","PeriodicalId":13743,"journal":{"name":"International immunology","volume":" ","pages":""},"PeriodicalIF":3.2,"publicationDate":"2026-04-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147698561","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Multiple evolutionary routes to immune diversification across animals.","authors":"Mizuki Taguchi, Sébastien de La Forest Divonne, Ryo Morimoto","doi":"10.1093/intimm/dxag018","DOIUrl":"https://doi.org/10.1093/intimm/dxag018","url":null,"abstract":"<p><p>Adaptive immunity is often viewed as a defining innovation of vertebrates, characterized by somatically diversified antigen-receptors and clonal lymphocyte lineages. Yet the evolutionary origins of such systems remain incompletely understood. In this review, we examine adaptive immunity from a comparative perspective across Metazoa, focusing on the design principles that link molecular diversification, immune cell differentiation, and proliferative dynamics. We first outline the two adaptive immune architectures found in vertebrates. Jawed vertebrates employ immunoglobulin-based and T cell receptor (TCR)-based recognition generated through RAG-mediated V(D)J recombination, whereas jawless vertebrates assemble variable lymphocyte receptors using cytidine-deaminase-dependent diversification of leucine-rich-repeat modules. Despite their distinct molecular entities, these systems converge on shared design principles, including somatic diversification, developmental restriction of genome editing, immune cell differentiation, and specialized microenvironments for immune education. To introduce evolutionarily more ancient systems, several diversification mechanisms of antigen-receptors in invertebrates will be subsequently surveyed. These systems generate substantial molecular diversity without canonical clonal selection, suggesting that immune recognition and diversification can be achieved through multiple evolutionary strategies. Particular attention is given to emerging insights into invertebrate immune cell diversification, where single-cell transcriptomics is revealing complex hematopoietic lineages and regulatory programs. These observations suggest that adaptive immunity did not emerge abruptly but rather represents one solution within a broader evolutionary landscape of immune diversification strategies. Understanding how diversification, proliferation, and cellular organization interact across animal lineages will help clarify the fundamental design constraints that shaped the evolution of vertebrate adaptive immune systems.</p>","PeriodicalId":13743,"journal":{"name":"International immunology","volume":" ","pages":""},"PeriodicalIF":3.2,"publicationDate":"2026-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147689448","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}