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(1) Effect of polysaccharides from a Korean ginseng berry on the immunosenescence of aged mice.[TOP]

Pubmed ID :30337804
Publication Date : //
Korean ginseng has been widely evaluated to treat human diseases; however, most studies on Korean ginseng have focused on its root. In this study, polysaccharides [acidic-polysaccharide-linked glycopeptide (APGP) extracted with 90% ethanol and hot water] were prepared from Korean ginseng berries, and their effect on immunosenescence was explored.

Authors : Kim Miseon, Yi Young-Su, Kim Juewon, Han Sang Yun, Kim Su Hwan, Seo Dae Bang, Cho Jae Youl, Shin Song Seok,

(2) Naringenin Modifies the Development of Lineage-Specific Effector CD4 T Cells.[TOP]

Pubmed ID :30327657
Publication Date : //
Disrupted balance in the lineages of CD4 T cell subsets, including pro-inflammatory T helper (Th) cells and anti-inflammatory regulatory T cells (Treg), is a primary pathogenic factor for developing autoimmunity. We have found that this immunomodulatory effect of naringenin on effector T cells and T-cell mediated experimental autoimmune encephalomyelitis (EAE). We therefore explored the effects of naringenin on the development of different effector CD4 T cells. Naïve CD4 T cells were differentiated under respective Th1, Th2, Th17, and Treg polarizing conditions with naringenin. Percent populations of each differentiated CD4 T cell subsets were determined and the corresponding regulating pathways were investigated as underlying mechanisms. Naringenin mainly inhibited CD4 T cell proliferation and differentiation to Th1 and Th17, but did not affect Th2 cells. Impeded Th1 polarization was associated with inhibition of its specific regulator proteins T-bet, p-STAT1, and p-STAT4 by naringenin. Likewise, Th17 regulator proteins RORγt, p-STAT3, and Ac-STAT3 were also inhibited by naringenin. In addition, naringenin promoted Treg polarization and also prevented IL-6-induced suppression of Treg development via down-regulation of p-Smad2/3 as well as inhibition of IL-6 signaling, and the latter was further supported by the results showing lower soluble IL-6R but higher soluble gp130 levels in plasma of naringenin-fed compared to the control EAE mice. Naringenin impacts CD4 T cell differentiation in a manner that would explain its beneficial effect in preventing/mitigating T cell-mediated autoimmunity.

Authors : Wang Junpeng, Niu Xinli, Wu Chunfang, Wu Dayong,

(3) Cross-Reactivity and Anti-viral Function of Dengue Capsid and NS3-Specific Memory T Cells Toward Zika Virus.[TOP]

Pubmed ID :30327651
Publication Date : //
Zika virus (ZIKV), a flavivirus with homology to dengue virus (DENV), is spreading to areas of DENV hyper-endemicity. Heterologous T cell immunity, whereby virus-specific memory T cells are activated by variant peptides derived from a different virus, can lead to enhanced viral clearance or diminished protective immunity and altered immunopathology. In mice, CD8+ T cells specific for DENV provide protective efficacy against subsequent ZIKV infection. In humans, contrasting studies report complete absence or varying degrees of DENV/ZIKV T cell cross-reactivity. Moreover, the impact of cross-reactive T cell recognition on the anti-viral capacity of T cells remains unclear. Here, we show that DENV-specific memory T cells display robust cross-reactive recognition of ZIKV NS3 and after expansion in respectively = 7/10 and = 9/9 dengue-immune individuals tested. In contrast, cross-reactivity toward ZIKV capsid is low or absent. Cross-reactive recognition of DENV or ZIKV NS3 peptides elicits similar production of the anti-viral effector mediators IFN-γ, TNF-α, and CD107a. We identify 9 DENV/ZIKV cross-reactive epitopes, 7 of which are CD4+ and 2 are CD8+ T cell epitopes. We also show that cross-reactive CD4+ and CD8+ T cells targeting novel NS3 epitopes display anti-viral effector potential toward ZIKV-infected cells, with CD8+ T cells mediating direct lyses of these cells. Our results demonstrate that DENV NS3-specific memory T cells display anti-viral effector capacity toward ZIKV, suggesting a potential beneficial effect in humans of pre-existing T cell immunity to DENV upon ZIKV infection.

Authors : Lim Mei Qiu, Kumaran Emmanuelle A P, Tan Hwee Cheng, Lye David C, Leo Yee Sin, Ooi Eng Eong, MacAry Paul A, Bertoletti Antonio, Rivino Laura,

(4) Targeting ulcerative colitis by suppressing glucose uptake with ritonavir.[TOP]

Pubmed ID :30322872
Publication Date : //
Glucose is the preferred source of energy in activated inflammatory cells. Glucose uptake into the cell is ensured by a family of glucose uptake transporters (GLUT) which have been identified as off target molecules of the HIV protease inhibitor ritonavir. In this study, we examined the effect of ritonavir on inflammation and Peripheral blood mononuclear cells (PBMC) were activated with anti CD3 in the presence or absence of ritonavir and analyzed by flow cytometric analysis. Frequencies of CD4+ cells were significantly affected by ritonavir (CD69+ p=3E-05; CD134 p=4E-06; CD25+ p= E-07; central memory p=0.02, effector p=6E-03; effector memory p=6E-05). To corroborate that inflammation has a metabolic effect a mouse model was used which is based on immunocompromised NOD-scid IL-2R γ mice reconstituted with PBMC from patients with ulcerative colitis (UC). Inflammation had a significant effect on amino acid (AS) levels (Glu p=1E-07, Asp p=1E-04). Principal component analysis (PCA) discriminated between unchallenged and challenged groups. Finally, the efficacy of ritonavir was tested in the same mouse model. Dependent variables were clinical- and histological scores, frequencies of human leukocytes isolated from spleen and colon and levels of AS in sera of mice. Mice benefited from treatment with ritonavir as indicated by significantly decreased colon- (p=7E-04) and histological (p=1E-04) scores, frequencies of M2 monocytes (CD14+ CD163), (p=0.02) and Glu levels (p=2E-05). PCA analysis discriminated between control and challenged groups (p=0.026). Thus, inhibition of glucose uptake might be a promising therapeutic intervention point for active UC.

Authors : Jodeleit Henrika, Al-Amodi Omar, Caesar Janina, Aguilera Christina Villarroel, Holdt Lesca, Gropp Roswitha, Beigel Florian, Siebeck Matthias,

(5) Interferon-γ-mediated Secretion of Tryptophanyl-tRNA Synthetases Has a Role in Protection of Human Umbilical Cord Blood-derived Mesenchymal Stem Cells Against Experimental Colitis.[TOP]

Pubmed ID :30293546
Publication Date : //
Mesenchymal stem cells (MSCs) are multipotent adult stem cells that present immunosuppressive effects in experimental and clinical trials targeting various rare diseases including inflammatory bowel disease (IBD). In addition, recent studies have reported tryptophanyl-tRNA synthetase (WRS) possess uncanonical roles such as angiostatic and anti-inflammatory effects. However, little is known about the function of WRS in MSC-based therapy. In this study, we investigated if a novel factor, WRS, secreted from MSCs has a role in amelioration of IBD symptoms and determined a specific mechanism underlying MSC therapy. Experimental colitis was induced by administration of 3% DSS solution to 8-week-old mice and human umbilical cord blood-derived MSCs (hUCB-MSCs) were injected intraperitoneally. Secretion of WRS from hUCB-MSCs and direct effect of WRS on isolated CD4+ T cells was determined via in vitro experiments and hUCB-MSCs showed significant therapeutic rescue against experimental colitis. Importantly, WRS level in serum of colitis induced mice decreased and recovered by administration of MSCs. Through in vitro examination, WRS expression of hUCB-MSCs increased when cells were treated with interferon-γ (IFN-γ). WRS was evaluated and revealed to have a role in inhibiting activated T cells by inducing apoptosis. In summary, IFN-γ-mediated secretion of WRS from MSCs has a role in suppressive effect on excessive inflammation and disease progression of IBD and brings new highlights in the immunomodulatory potency of hUCB-MSCs.

Authors : Kang Insung, Lee Byung-Chul, Lee Jin Young, Kim Jae-Jun, Lee Seung-Eun, Shin Nari, Choi Soon Won, Kang Kyung-Sun,

(6) LDH-A regulates the tumor microenvironment via HIF-signaling and modulates the immune response.[TOP]

Pubmed ID :30248111
Publication Date : //
Previous studies show that LDH-A knockdown reduces orthotopic 4T1 breast tumor lactate and delays tumor growth and the development of metastases in nude mice. Here, we report significant changes in the tumor microenvironment (TME) and a more robust anti-tumor response in immune competent BALB/c mice. 4T1 murine breast cancer cells were transfected with shRNA plasmids directed against LDH-A (KD) or a scrambled control plasmid (NC). Cells were also transduced with dual luciferase-based reporter systems to monitor HIF-1 activity and the development of metastases by bioluminescence imaging, using HRE-sensitive and constitutive promoters, respectively. The growth and metastatic profile of orthotopic 4T1 tumors developed from these cell lines were compared and a primary tumor resection model was studied to simulate the clinical management of breast cancer. Primary tumor growth, metastasis formation and TME phenotype were significantly different in LDH-A KD tumors compared with controls. In LDH-A KD cells, HIF-1 activity, hexokinase 1 and 2 expression and VEGF secretion were reduced. Differences in the TME included lower HIF-1α expression that correlated with lower vascularity and pimonidazole staining, higher infiltration of CD3+ and CD4+ T cells and less infiltration of TAMs. These changes resulted in a greater delay in metastases formation and 40% long-term survivors (>20 weeks) in the LDH-A KD cohort following surgical resection of the primary tumor. We show for the first time that LDH-depletion inhibits the formation of metastases and prolongs survival of mice through changes in tumor microenvironment that modulate the immune response. We attribute these effects to diminished HIF-1 activity, vascularization, necrosis formation and immune suppression in immune competent animals. Gene-expression analyses from four human breast cancer datasets are consistent with these results, and further demonstrate the link between glycolysis and immune suppression in breast cancer.

Authors : Serganova Inna, Cohen Ivan J, Vemuri Kiranmayi, Shindo Masahiro, Maeda Masatomo, Mane Mayuresh, Moroz Ekaterina, Khanin Raya, Satagopan Jaya, Koutcher Jason A, Blasberg Ronald,

(7) Interleukin-9 Blockade Suppresses Silica-induced Lung Inflammation and Fibrosis in Mice.[TOP]

Pubmed ID :30240278
Publication Date : //
Recapitulative animal models of idiopathic pulmonary fibrosis (IPF) and related diseases are lacking, which inhibits our ability to fully clarify the pathogenesis of these diseases. Although lung fibrosis in mouse models is often induced by bleomycin, silica-induced lung fibrosis is more sustainable and more progressive. Therefore, in this study, we sought to elucidate the mediator(s) responsible for the pathogenesis of lung fibrosis through the use of a mouse model of silica-induced lung fibrosis. With a single nasal administration of 16 mg of silica, lung inflammation (assessed by elevated cellular components in the bronchoalveolar lavage fluids [BALFs]) and lung fibrosis (assessed by lung histology and lung hydroxyproline levels) were induced and sustained for as long as 24 weeks. Of the mediators measured in the BALFs, interleukin-9 (IL-9) was characteristically elevated gradually and peaked at 24 weeks after silica administration. Treatment of silica-challenged mice with anti-IL-9 neutralizing Ab inhibited lung fibrosis, as assessed by lung hydroxyproline level, and suppressed the levels of major mediators, including IL-1β, IL-6, IL-12, CCL2, CXCL1, and tumor necrosis factor α in BALFs. Moreover, human lung specimens from IPF patients have shown high expression of IL-9 in alveolar macrophages, CD4-positive cells, and receptors for IL-9 in airway epithelial cells. Collectively, these data suggest that IL-9 plays an important role in the pathogenesis of lung fibrosis in diseases such as IPF.

Authors : Sugimoto Naoya, Suzukawa Maho, Nagase Hiroyuki, Koizumi Yuta, Ro Shoki, Kobayashi Konomi, Yoshihara Hisanao, Kojima Yasuhiro, Kamiyama-Hara Asae, Hebisawa Akira, Ohta Ken,

(8) Hypersensitivity reactions to asparaginase in mice are mediated by anti-asparaginase IgE and IgG and the immunoglobulin receptors FcϵRI and FcγRIII.[TOP]

Pubmed ID :30237274
Publication Date : //
Asparaginase is an important drug for the treatment of leukemias. However, anti-asparaginase antibodies often develop, which can decrease asparaginase drug levels and increase the risk of relapse. The aim of this study is to identify the immunoglobulin isotypes and receptors responsible for asparaginase hypersensitivities. Mice immunized with asparaginase developed anti-asparaginase IgG1 and IgE antibodies, and challenging the sensitized mice with asparaginase induced severe hypersensitivity reactions. Flow cytometry analysis indicated that macrophages/monocytes, neutrophils, and basophils bind asparaginase ex vivo through FcγRIII. In contrast, asparaginase binding to basophils was dependent on FcγRIII and IgE. Consistent with the asparaginase binding data, basophil activation by asparaginase occurred via both IgG/FcγRIII and IgE/FcϵRI. Depleting >95% of B cells suppressed IgG but not IgE-dependent hypersensitivity, while depleting CD4+ T cells provided complete protection. Combined treatment with either anti-IgE mAb plus a platelet-activating factor receptor antagonist or anti-FcγRIII mAb plus a H1 receptor antagonist suppressed asparaginase hypersensitivity. The observations indicate that asparaginase hypersensitivity is mediated by antigen-specific IgG and/or IgE through the immunoglobulin receptors FcγRIII and FcϵRI, respectively. Provided that these results apply to humans, they emphasize the importance of monitoring both IgE- and IgG-mediated asparaginase hypersensitivities in patients receiving this agent.

Authors : Rathod Sanjay, Ramsey Manda, Relling Mary V, Finkelman Fred D, Fernandez Christian A,

(9) Single-cell transcriptomics reveal that PD-1 mediates immune tolerance by regulating proliferation of regulatory T cells.[TOP]

Pubmed ID :30236153
Publication Date : //
We have previously reported an antigen-specific protocol to induce transplant tolerance and linked suppression to human embryonic stem cell (hESC)-derived tissues in immunocompetent mice through coreceptor and costimulation blockade. However, the exact mechanisms of acquired immune tolerance in this model have remained unclear.

Authors : Leung Cherry S, Yang Kevin Y, Li Xisheng, Chan Vicken W, Ku Manching, Waldmann Herman, Hori Shohei, Tsang Jason C H, Lo Yuk Ming Dennis, Lui Kathy O,

(10) Mesenchymal stem cells alleviate experimental autoimmune cholangitis through immunosuppression and cytoprotective function mediated by galectin-9.[TOP]

Pubmed ID :30223894
Publication Date : //
Mesenchymal stem cells (MSCs) play an anti-inflammatory role by secreting certain bioactive molecules to exert their therapeutic effects for disease treatment. However, the underlying mechanism of MSCs in chronic autoimmune liver diseases-primary biliary cholangitis (PBC), for example-remains to be elucidated.

Authors : Fan Junyu, Tang Xiaojun, Wang Qian, Zhang Zhuoya, Wu Shufang, Li Wenchao, Liu Shanshan, Yao Genhong, Chen Hongwei, Sun Lingyun,