Publications by authors named "Jun Gui"

14 Publications

  • Page 1 of 1

[Study on chemical bibenzyls in Dendrobium gratiosissimum].

Zhongguo Zhong Yao Za Zhi 2020 Oct;45(20):4929-4937

State Key Laboratory of Bioactive Substance and Function of Natural Medicines,Key Laboratory of Natural Drug Biosynthesis of National Health Committee,Key Laboratory of Enzymes and Natural Drug Biocatalysis of Chinese Academy of Medical Sciences,Institute of Materia Medica,Chinese Academy of Medical Sciences & Peking Union Medical College Beijing 100050,China.

Nineteen compounds were isolated and structurally characterized from an ethanol extract of Dendrobium gratiossimum, including dendrogratiol A(1), DDB-1(2), 3,4-dihydroxyl-5,3',4'-trimethoxybibenzyl(3), amoenylin(4), chrysotoxine(5), DTB(6), 3,4,4'-trihydroxyl-5,3'-dimethoxybenzyl(7), 3-methylgiga(8), aloifol(9), gigantol tetramethyl ether(10), batatasin Ⅲ(11), moscatilin(12), moniliformine(13), gigantol(14), DMB(15), flavanthrinin(16), cannithrene-2(17), 3,4-dihydroxyl-5,4'-dimethoxystilbene(18) and 4-hydroxy-3,5,4'-trimethoxystilbene(19). 1 was a new compound, and 2-10, 16, 18 and 19 were obtained from this plant species for the first time. In vitro cytotoxic and antiviral activities of these isolates were evaluated, which displayed that 4 showed moderate cytotoxicity against human hepatoma cell line HepG2 with the IC_(50) of 10.15 μmol·L~(-1); 7 and 12 exhibited moderate inhibitory activity towards HIV virus with the IC_(50) of 9.35 and 9.15 μmol·L~(-1), respectively; and 10 displayed inhibitory activity against IAV virus with the IC_(50) of 8.90 μmol·L~(-1).
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http://dx.doi.org/10.19540/j.cnki.cjcmm.20200523.201DOI Listing
October 2020

Cancer-associated fibroblasts downregulate type I interferon receptor to stimulate intratumoral stromagenesis.

Oncogene 2020 09 17;39(38):6129-6137. Epub 2020 Aug 17.

Department of Biomedical Sciences, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, PA, 19104, USA.

Activation of cancer-associated fibroblasts (CAFs) and ensuing desmoplasia play an important role in the growth and progression of solid tumors. Here we demonstrate that, within colon and pancreatic ductal adenocarcinoma tumors, efficient stromagenesis relies on downregulation of the IFNAR1 chain of the type I interferon (IFN1) receptor. Expression of the fibroblast activation protein (FAP) and accumulation of the extracellular matrix (ECM) was notably impaired in tumors grown in the Ifnar1 (SA) knock-in mice, which are deficient in IFNAR1 downregulation. Primary fibroblasts from these mice exhibited elevated levels of Smad7, a negative regulator of the transforming growth factor-β (TGFβ) pathway. Knockdown of Smad7 alleviated deficient ECM production in SA fibroblasts in response to TGFβ. Analysis of human colorectal cancers revealed an inverse correlation between IFNAR1 and FAP levels. Whereas growth of tumors in SA mice was stimulated by co-injection of wild type but not SA fibroblasts, genetic ablation of IFNAR1 in fibroblasts also accelerated tumor growth. We discuss how inactivation of IFNAR1 in CAFs acts to stimulate stromagenesis and tumor growth.
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http://dx.doi.org/10.1038/s41388-020-01424-7DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7502515PMC
September 2020

Dynamics of calling activity to toll-free numbers in China.

PLoS One 2020 26;15(3):e0230592. Epub 2020 Mar 26.

Shenyang Institute of Automation, Chinese Academy of Sciences, Shenyang, China.

The quantitative understanding of human behavior is a key issue in modern science. Recently, inhomogeneous human activities have been described by bursts (consecutive activities separated by long periods of inactivity) and characterized by fat-tailed inter-event time (interval between two activities) distributions. However, the dynamics between number of activities and activity duration are still unclear. In this study, we analyzed 133 million toll-free call records from China to study the dynamics between call frequency and call duration. We confirmed that both call frequency and call duration exhibit circadian cycles and weekly cycles. By analyzing intraday patterns of these two metrics, we found the opposite volatility and clustered distributions. Results of clustering analysis showed that calling activity to toll-free numbers can be clustered into four clusters. In the "Work" cluster, the distribution of call duration was significantly different from that in the other clusters. The corresponding time of "Work" cluster was much shorter than estimates based on common sense. Intraday patterns and clustering results showed that both call frequency and call duration are primarily related to circadian cycles, the nature of human beings, and that work is a secondary factor that affects these variables. Moreover, we found a strong positive correlation between call frequency and call duration, as well as polarization of joint probability. The polarization indicates two extremes in inhomogeneous calling activity to toll-free numbers, i.e., either people are very busy or very idle. The empirical probability of the extreme was approximately four times that of random probability. Our findings may have great usage for studying the dynamics of inhomogeneous human behavior.
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http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0230592PLOS
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7098560PMC
June 2020

The PKR-Like Endoplasmic Reticulum Kinase Promotes the Dissemination of Myc-Induced Leukemic Cells.

Mol Cancer Res 2019 07 22;17(7):1450-1458. Epub 2019 Mar 22.

Department of Biomedical Sciences, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, Pennsylvania.

Hyperactive oncogenic Myc stimulates protein synthesis that induces the unfolded protein response, which requires the function of the eukaryotic translation initiation factor 2-alpha kinase 3, also known as protein kinase R (PKR)-like endoplasmic reticulum kinase (PERK). Activated PERK acts to limit mRNA translation, enable proper protein folding, and restore the homeostasis in the endoplasmic reticulum. Given that Myc activation contributes to many types of lymphoid and myeloid human leukemias, we used a mouse model to examine the importance of PERK in development and progression of Myc-induced leukemias. We found that genetic ablation of does not suppress the generation of the leukemic cells in the bone marrow. However, the cell-autonomous deficiency restricts the dissemination of leukemic cells into peripheral blood, lymph nodes, and vital peripheral organs. Whereas the loss of the IFNAR1 chain of type I IFN receptor stimulated leukemia, ablation did not stabilize IFNAR1, suggesting that PERK stimulates the leukemic cells' dissemination in an IFNAR1-independent manner. We discuss the rationale for using PERK inhibitors against Myc-driven leukemias. IMPLICATIONS: The role of PERK in dissemination of Myc-induced leukemic cells demonstrated in this study argues for the use of PERK inhibitors against leukemia progression.
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http://dx.doi.org/10.1158/1541-7786.MCR-19-0002DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6610583PMC
July 2019

An Interferon-Driven Oxysterol-Based Defense against Tumor-Derived Extracellular Vesicles.

Cancer Cell 2019 01;35(1):33-45.e6

Department of Biomedical Sciences, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA. Electronic address:

Tumor-derived extracellular vesicles (TEV) "educate" healthy cells to promote metastases. We found that melanoma TEV downregulated type I interferon (IFN) receptor and expression of IFN-inducible cholesterol 25-hydroxylase (CH25H). CH25H produces 25-hydroxycholesterol, which inhibited TEV uptake. Low CH25H levels in leukocytes from melanoma patients correlated with poor prognosis. Mice incapable of downregulating the IFN receptor and Ch25h were resistant to TEV uptake, TEV-induced pre-metastatic niche, and melanoma lung metastases; however, ablation of Ch25h reversed these phenotypes. An anti-hypertensive drug, reserpine, suppressed TEV uptake and disrupted TEV-induced formation of the pre-metastatic niche and melanoma lung metastases. These results suggest the importance of CH25H in defense against education of normal cells by TEV and argue for the use of reserpine in adjuvant melanoma therapy.
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http://dx.doi.org/10.1016/j.ccell.2018.12.001DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6336114PMC
January 2019

Targeting Myeloid-derived Suppressor Cells and Programmed Death Ligand 1 Confers Therapeutic Advantage of Ablative Hypofractionated Radiation Therapy Compared With Conventional Fractionated Radiation Therapy.

Int J Radiat Oncol Biol Phys 2018 05 12;101(1):74-87. Epub 2018 Mar 12.

Department of Thoracic Oncology, Cancer Center and State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, China. Electronic address:

Purpose: Ablative hypofractionated radiation therapy (AHFRT) presents a therapeutic advantage compared with conventional fractionated radiation therapy (CFRT) for primary and oligometastatic cancers. However, the underlying mechanisms remain largely unknown. In the present study, we compared the immune alterations in response to AHFRT versus CFRT and examined the significance of immune regulations contributing to the efficacy of AHFRT.

Methods And Materials: We established subcutaneous tumors using syngeneic lung cancer and melanoma cells in both immunocompetent and immunocompromised mice and treated them with AHFRT and CFRT under the same biologically equivalent dose.

Results: Compared with CFRT, AHFRT significantly inhibited tumor growth in immunocompetent, but not immunocompromised, mice. On the cellular level, AHFRT reduced the recruitment of myeloid-derived suppressor cells (MDSCs) into tumors and decreased the expression of programmed death-ligand 1 (PD-L1) on those cells, which unlashed the cytotoxicity of CD8 T cells. Through the downregulation of vascular endothelial growth factor (VEGF), AHFRT inhibited VEGF/VEGF receptor signaling, which was essential for MDSC recruitment. When combined with anti-PD-L1 antibody, AHFRT presented with greater efficacy in controlling tumor growth and improving mouse survival. By altering immune regulation, AHFRT, but not CFRT, significantly delayed the growth of secondary tumors implanted outside the irradiation field.

Conclusions: Targeting MDSC recruitment and enhancing antitumor immunity are crucial for the therapeutic efficacy of AHFRT. When combined with anti-PD-L1 immunotherapy, AHFRT was more potent for cancer treatment.
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http://dx.doi.org/10.1016/j.ijrobp.2018.01.071DOI Listing
May 2018

Downregulation of the IFNAR1 chain of type 1 interferon receptor contributes to the maintenance of the haematopoietic stem cells.

Cancer Biol Ther 2017 Jul 5;18(7):534-543. Epub 2017 Jul 5.

a Department of Biomedical Sciences and Mari Lowe Center for Comparative Oncology , School of Veterinary Medicine, University of Pennsylvania , Philadelphia , PA , USA.

Recent studies demonstrated that prolonged exposure of haematopoietic stem cells (HSCs) to type I interferons (IFN) stimulates HSCs entrance into cell cycle, continuous proliferation and eventual exhaustion, which could be prevented by ablation of the Ifnar1 chain of IFN receptor. Given that levels IFNAR1 expression can be robustly affected by IFN-independent ubiquitination and downregulation of IFNAR1 in response to activation of protein kinases such as protein kinase R-like endoplasmic reticulum kinase (PERK) and casein kinase 1α (CK1α), we aimed to determine the role of IFNAR1 downregulation in the maintenance of HSCs. Mice harboring the ubiquitination-deficient Ifnar1 allele displayed greater levels of haematopoietic cell progenitors but reduced numbers of the long-term HSCs compared with wild type mice and animals lacking Ifnar1. Studies using competitive bone marrow repopulation assays showed that CK1α (but not PERK) is essential for the long-term HSCs function. Concurrent ablation of Ifnar1 led to a modest attenuation of the CK1α-null phenotype indicating that, although other CK1α targets are likely to be important, IFNAR1 downregulation can contribute to the maintenance of the HSCs function.
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http://dx.doi.org/10.1080/15384047.2017.1345395DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5639844PMC
July 2017

Inactivation of Interferon Receptor Promotes the Establishment of Immune Privileged Tumor Microenvironment.

Cancer Cell 2017 02;31(2):194-207

Department of Biomedical Sciences, Mari Lowe Center for Comparative Oncology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA. Electronic address:

Refractoriness of solid tumors, including colorectal cancers (CRCs), to immunotherapies is attributed to the immunosuppressive tumor microenvironment that protects malignant cells from cytotoxic T lymphocytes (CTLs). We found that downregulation of the type I interferon receptor chain IFNAR1 occurs in human CRC and mouse models of CRC. Downregulation of IFNAR1 in tumor stroma stimulated CRC development and growth, played a key role in formation of the immune-privileged niche, and predicted poor prognosis in human CRC patients. Genetic stabilization of IFNAR1 improved CTL survival and increased the efficacy of the chimeric antigen receptor T cell transfer and PD-1 inhibition. Likewise, pharmacologic stabilization of IFNAR1 suppressed tumor growth providing the rationale for upregulating IFNAR1 to improve anti-cancer therapies.
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http://dx.doi.org/10.1016/j.ccell.2017.01.004DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5313042PMC
February 2017

Therapeutic Elimination of the Type 1 Interferon Receptor for Treating Psoriatic Skin Inflammation.

J Invest Dermatol 2016 10 29;136(10):1990-2002. Epub 2016 Jun 29.

Department of Biomedical Sciences, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA. Electronic address:

Phototherapy with UV light is a standard treatment for psoriasis, yet the mechanisms underlying the therapeutic effects are not well understood. Studies in human and mouse keratinocytes and in the skin tissues from human patients and mice showed that UV treatment triggers ubiquitination and downregulation of the type I IFN receptor chain IFNAR1, leading to suppression of IFN signaling and an ensuing decrease in the expression of inflammatory cytokines and chemokines. The severity of imiquimod-induced psoriasiform inflammation was greatly exacerbated in skin of mice deficient in IFNAR1 ubiquitination (Ifnar1(SA)). Furthermore, these mice did not benefit from UV phototherapy. Pharmacologic induction of IFNAR1 ubiquitination and degradation by an antiprotozoal agent halofuginone also relieved psoriasiform inflammation in wild-type but not in Ifnar1(SA) mice. These data identify downregulation of IFNAR1 by UV as a major mechanism of the UV therapeutic effects against the psoriatic inflammation and provide a proof of principle for future development of agents capable of inducing IFNAR1 ubiquitination and downregulation for the treatment of psoriasis.
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http://dx.doi.org/10.1016/j.jid.2016.06.608DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5035634PMC
October 2016

Type I interferons mediate pancreatic toxicities of PERK inhibition.

Proc Natl Acad Sci U S A 2015 Dec 1;112(50):15420-5. Epub 2015 Dec 1.

Department of Animal Biology, School of Veterinary Medicine, Philadelphia, PA 19104;

The great preclinical promise of the pancreatic endoplasmic reticulum kinase (PERK) inhibitors in neurodegenerative disorders and cancers is marred by pancreatic injury and diabetic syndrome observed in PERK knockout mice and humans lacking PERK function and suffering from Wolcott-Rallison syndrome. PERK mediates many of the unfolded protein response (UPR)-induced events, including degradation of the type 1 interferon (IFN) receptor IFNAR1 in vitro. Here we report that whole-body or pancreas-specific Perk ablation in mice leads to an increase in IFNAR1 protein levels and signaling in pancreatic tissues. Concurrent IFNAR1 deletion attenuated the loss of PERK-deficient exocrine and endocrine pancreatic tissues and prevented the development of diabetes. Experiments using pancreas-specific Perk knockouts, bone marrow transplantation, and cultured pancreatic islets demonstrated that stabilization of IFNAR1 and the ensuing increased IFN signaling in pancreatic tissues represents a major driver of injury triggered by Perk loss. Neutralization of IFNAR1 prevented pancreatic toxicity of PERK inhibitor, indicating that blocking the IFN pathway can mitigate human genetic disorders associated with PERK deficiency and help the clinical use of PERK inhibitors.
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http://dx.doi.org/10.1073/pnas.1516362112DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4687574PMC
December 2015

Remission of CVB3-induced myocarditis with Astragaloside IV treatment requires A20 (TNFAIP3) up-regulation.

J Cell Mol Med 2015 Apr 1;19(4):850-64. Epub 2015 Mar 1.

Institute for Immunobiology, Shanghai Medical College, Fudan University, Shanghai, China.

Viral myocarditis (VMC) most prevalently caused by coxsackievirus B3 (CVB3) infection is characterized by severe cardiac inflammation. Therapeutic options for the disease are still limited. Astragaloside IV (AST-IV), a purified small molecular saponin (C41 H68 O14 , MW 784), is the main active component of Chinese medical herb Astragalus which has been empirically prescribed for the treatment of heart dysfunction for centuries. In this study, we investigated the effect of AST-IV on CVB3-induced myocarditis and explored its possible mechanism involved. The results showed that AST-IV administration alleviated the severity of myocarditis and attenuated cardiac inflammation, which was mediated by inhibition of nuclear factor-kappaB (NF-κB) signalling. Importantly, we further identified that the inhibitory effect of AST-IV on NF-κB signalling was through increasing A20 (TNFAIP3) expression. Moreover, we validated that A20 was critical for the therapeutic efficacy of AST-IV on CVB3-induced myocarditis. Finally, we revealed that AST-IV enhanced A20 expression at post-transcriptional level by stabilization of mRNA. Our findings uncover a previously unknown mechanism for AST-IV in the treatment of VMC because of modulating inflammatory response via increasing A20 expression, which provide a potential target for screening new drugs and are helpful for optimization of the therapeutic strategies for VMC.
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http://dx.doi.org/10.1111/jcmm.12459DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4395199PMC
April 2015

A20 (TNFAIP3) alleviates CVB3-induced myocarditis via inhibiting NF-κB signaling.

PLoS One 2012 28;7(9):e46515. Epub 2012 Sep 28.

Institute for Immunobiology, Shanghai Medical College, Fudan University, Shanghai, People's Republic of China.

Background: Viral myocarditis, which is most prevalently caused by Coxsackievirus B3 (CVB3) infection, is a serious clinical condition characterized by cardiac inflammation. However, efficient therapies targeting inflammation are still lacking and much needed. A20, also known as tumor necrosis factor alpha induced protein 3 (TNFAIP3) is a key negative regulator of inflammation. But whether A20 may affect cardiac inflammation during acute viral myocarditis remains to be elucidated. The aim of this study was to investigate the potential protective effect of A20 on CVB3-induced myocarditis.

Methodology/principal Findings: Mice were intraperitoneally inoculated with CVB3 to establish acute viral myocarditis model. We found that the expression of pro-inflammatory cytokines, including tumor necrosis factor-α (TNF-α), interleukin (IL)-1β, IL-6 and monocyte chemotactic protein-1 (MCP-1) were markedly and persistently increased during the progression of CVB3-induced myocarditis, and positively correlated with the disease severity. Notably, intravenous injection in vivo with adenovirus expressed A20 (Ad-A20) remarkably reduced CVB3-induced pro-inflammatory cytokines production and alleviated the severity of myocarditis. Further, we observed that nuclear factor-kappaB (NF-κB) signaling which mediates inflammatory response was significantly inhibited in CVB3-infected mice with Ad-A20 treatment. Finally, we revealed that A20 was required to inhibit CVB3-induced NF-κB signaling by restricting TNF receptor associated factor 6 (TRAF6) ubiquitylation.

Conclusion/significance: This study demonstrates the protective role of A20 against CVB3-induced myocarditis, which may provide a new therapeutic strategy for the treatment of viral myocarditis.
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http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0046515PLOS
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3460927PMC
February 2013

Direct gene transfer with IP-10 mutant ameliorates mouse CVB3-induced myocarditis by blunting Th1 immune responses.

PLoS One 2011 Mar 22;6(3):e18186. Epub 2011 Mar 22.

Laboratory of Infection and Immunity, Institutes of Biology and Medical Sciences, Soochow University, Suzhou, People's Republic of China.

Background: Myocarditis is an inflammation of the myocardium that often follows the enterovirus infections, with coxsackievirus B3 (CVB3) being the most dominant etiologic agent. We and other groups previously reported that chemokine IP-10 was significantly induced in the heart tissue of CVB3-infected mice and contributed to the migration of massive inflammatory cells into the myocardium, which represents one of the most important mechanisms of viral myocarditis. To evaluate the direct effect of IP-10 on the inflammatory responses in CVB3 myocarditis, herein an IP-10 mutant deprived of chemo-attractant function was introduced into mice to antagonize the endogenous IP-10 activity, and its therapeutic effect on CVB3-induced myocarditis was evaluated.

Methodology/principal Findings: The depletion mutant pIP-10-AT, with an additional methionine after removal of the 5 N-terminal amino acids, was genetically constructed and intramuscularly injected into BALB/c mice after CVB3 infection. Compared with vector or no treatment, pIP-10-AT treatment had significantly reduced heart/body weight ratio and serum CK-MB level, increased survival rate and improved heart histopathology, suggesting an ameliorated myocarditis. This therapeutic effect was not attributable to an enhanced viral clearance, but to a blunted Th1 immune response, as evidenced by significantly decreased splenic CD4(+)/CD8(+)IFN-γ(+) T cell percentages and reduced myocardial Th1 cytokine levels.

Conclusion/significance: Our findings constitute the first preclinical data indicating that interfering in vivo IP-10 activity could ameliorate CVB3 induced myocarditis. This strategy may represent as a new therapeutic approach in treating viral myocarditis.
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http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0018186PLOS
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3062568PMC
March 2011

Gene therapy with CCL2 (MCP-1) mutant protects CVB3-induced myocarditis by compromising Th1 polarization.

Mol Immunol 2011 Jan 17;48(4):706-13. Epub 2010 Dec 17.

Laboratory of Infection and Immunity, Institute of Biology and Medical Sciences, Soochow University, 199 Ren-Ai Road, Suzhou 215123, PR China.

Viral myocarditis, which is most prevalently caused by Coxsackievirus B3 (CVB3) infection, affects about 5-20% of the world population and lacks efficient treatments. We previously reported that monocyte chemotactic protein-1 (MCP-1, CCL2) was significantly induced during CVB3 infection and greatly contributed to the myocardic inflammation and injury. Herein a CCL2 mutant with removed chemotactic activity was administrated and its therapeutic effect on CVB3-induced myocarditis was explored. A dominant negative CCL2 mutant, lacking the N-terminal amino acids 2-8 (CCL2(Δ2-8)), was genetically constructed and intramuscularly injected into BALB/c mice after CVB3 infection, severity of myocarditis was evaluated by weight loss, survival rate, serological indices and pathological observation. Systemic and local Th1/Th2 cytokine profiles were also assessed. Mice receiving pCCL2(Δ2-8) exhibited a profound attenuation of myocarditis compared to pcDNA3.1 or non-treated mice, as evidenced by invariant body weight, decreased serum CK-MB level, reduced myocardial inflammatory infiltration and increased survival. This effect was not attributable to the efficient viral clearance, but associated with weakened Th1 immune responses, as evidenced by significantly reduced CD4(+)IFN-γ(+) T cell frequency and Th1 cytokine level systemically and locally. Strategy of blocking in vivo CCL2 activity could effectively alleviate the severity of CVB3-induced myocarditis and may present an alternative therapeutic approach against viral myocarditis.
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http://dx.doi.org/10.1016/j.molimm.2010.11.018DOI Listing
January 2011