Database : MEDLINE
Search on : granulocyte-macrophage and colony-stimulating and factor [Words]
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[PMID]: 29517628
[Au] Autor:Rodriguez-Nicolas A; Martínez-Chamorro A; Jiménez P; Matas-Cobos AM; Redondo-Cerezo E; Ruiz-Cabello F
[Ti] Title:TH1 and TH2 Cytokine Profiles as Predictors of Severity in Acute Pancreatitis.
[So] Source:Pancreas;47(4):400-405, 2018 Apr.
[Is] ISSN:1536-4828
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:OBJECTIVES: Acute pancreatitis (AP) is severe in up to 20% of patients, with a high mortality rate. Quantification of serum TH1 and TH2 cytokines may provide objective evidence to assess the severity of AP and predict its course. METHODS: One hundred seventeen patients were studied, measuring serum concentrations of interleukin (IL)1ß, IL2, IL4, IL5, IL6, IL10, IL12p70, IL13, IL18, granulocyte-macrophage colony-stimulating factor (GM-CSF), interferon (IFN) γ, and tumor necrosis factor (TNF) α. RESULTS: Significant differences were found between patients with severe AP and those with mild or moderately severe AP in IFN-γ (P < 0.001), IL6 (P < 0.001), TNF-α (P = 0.002), GM-CSF (P < 0.001), IL4 (P = 0.002), IL1b (P = 0.017), and IL13 (P < 0.001) concentrations. Interferon-γ, IL6, and TNF-α were associated with severe AP, whereas GM-CSF, IL4, IL1b, and IL13 were associated with mild or moderately severe AP. The IL13/IFNγ ratio was significantly higher in patients with mild AP (P = 7.36 × 10). CONCLUSIONS: A TH1 profile was associated with severe AP and a TH2 profile with mild or moderately severe AP. We report an IL13/IFNγ ratio of potential value to predict the prognosis in AP.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:In-Data-Review
[do] DOI:10.1097/MPA.0000000000001006

  2 / 18762 MEDLINE  
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[PMID]: 29458209
[Au] Autor:Abbas H; Kamel R; El-Sayed N
[Ad] Address:Pharmaceutics Department, Faculty of Pharmacy, Damanhour University, Egypt.
[Ti] Title:Dermal anti-oxidant, anti-inflammatory and anti-aging effects of Compritol ATO-based Resveratrol colloidal carriers prepared using mixed surfactants.
[So] Source:Int J Pharm;541(1-2):37-47, 2018 Feb 17.
[Is] ISSN:1873-3476
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:In this study, Compritol ATO-based Resveratrol colloidal carriers (CCCs) were prepared and subjected to characterization and evaluation. In most formulae, the use of a binary-mixture of surfactants improved the physicochemical properties. CCC6 (containing P407/P188 as bi-surfactants) attained the highest drug loading, release efficiency during 24 h and occlusive effect for 48 h; in addition, it showed a uniform particle size distribution within the desired range. In-vivo studies were done based on the analysis of anti-oxidant markers [catalase (CAT), reduced glutathione (GSH) and superoxide dismutase (SOD)], anti-inflammatory markers [interleukin 6 (IL-6), interleukin 8 (IL-8) and rat Nuclear factor-kappa B (NF-κB)] and anti-wrinkling markers [matrix metalloproteinase (MMP-1) and Granulocyte-macrophage colony-stimulating factor (GM-CSF)], after UVB-irradiation. Results were significantly different when comparing the positive control and the negative control groups (p < 0.05). Rats pre-treated with CCC6 showed a great amelioration, and the level of the biochemical markers was significantly different compared to those of the positive control group and those pre-treated with the drug suspension (p < 0.05). Also, the high skin protective effect of CCC6 was proved by visual and histopathological examination of the rats' skin. Therefore, the current study proves the beneficial effects of the designed dermal Resveratrol-loaded colloidal system.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180308
[Lr] Last revision date:180308
[St] Status:Publisher

  3 / 18762 MEDLINE  
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[PMID]: 29377076
[Au] Autor:Phoomvuthisarn P; Cross A; Glennon-Alty L; Wright HL; Edwards SW
[Ad] Address:Faculty of Veterinary Science, Chulalongkorn University, Bangkok, Thailand.
[Ti] Title:The CDK inhibitor purvalanol A induces neutrophil apoptosis and increases the turnover rate of Mcl-1: potential role of p38-MAPK in regulation of Mcl-1 turnover.
[So] Source:Clin Exp Immunol;, 2018 Jan 29.
[Is] ISSN:1365-2249
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Human neutrophils are terminally differentiated cells that do not replicate and yet express a number of enzymes, notably cell cycle-dependent kinases (CDKs), that are associated normally with control of DNA synthesis and cell cycle progression. In neutrophils, CDKs appear to function mainly to regulate apoptosis, although the mechanisms by which they regulate this process are largely unknown. Here we show that the CDK2 inhibitor, purvalanol A, induces a rapid decrease in myeloid cell leukaemia factor-1 (Mcl-1) levels in human neutrophils and peripheral blood mononuclear cells (PBMCs), but only induces apoptosis in neutrophils which are dependent upon expression on this protein for survival. This rapid decrease in cellular Mcl-1 protein levels was due to a purvalanol A-induced decrease in stability, with the half-life of the protein decreasing from approximately 2 h in control cells to just over 1 h after addition of the CDK2 inhibitor: it also blocked the granulocyte-macrophage colony-stimulating factor (GM-CSF)-dependent stabilization of Mcl-1. Purvanalol A blocked GM-CSF-stimulated activation of extracellular-regulated kinase (Erk) and signal transducer and activator of transcription (STAT)-3, and stimulated an additive activation of protein kinase B (Akt) with GM-CSF. Purvalanol A alone stimulated a rapid and sustained activation of p38-mitogen-activated protein kinase (MAPK) and the pan p38-MAPK inhibitor, BIRB796, partly blocked the purvalanol A-induced apoptosis and Mcl-1 loss. These novel effects of purvalanol A may result, at least in part, from blocking GM-CSF-mediated Erk activation. In addition, we propose that purvalanol A-induced activation of p38-MAPK is, at least in part, responsible for its rapid effects on Mcl-1 turnover and acceleration of neutrophil apoptosis.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1801
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:Publisher
[do] DOI:10.1111/cei.13107

  4 / 18762 MEDLINE  
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[PMID]: 29376889
[Au] Autor:Ullrich E; Abendroth B; Rothamer J; Huber C; Büttner-Herold M; Buchele V; Vogler T; Longerich T; Zundler S; Völkl S; Beilhack A; Rose-John S; Wirtz S; Weber GF; Ghimire S; Kreutz M; Holler E; Mackensen A; Neurath MF; Hildner K
[Ad] Address:Department of Medicine 5, University Hospital Erlangen, University of Erlangen-Nuremberg, Erlangen, Germany.
[Ti] Title:BATF-dependent IL-7RhiGM-CSF+ T cells control intestinal graft-versus-host disease.
[So] Source:J Clin Invest;128(3):916-930, 2018 Mar 01.
[Is] ISSN:1558-8238
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Acute graft-versus-host disease (GVHD) represents a severe, T cell-driven inflammatory complication following allogeneic hematopoietic cell transplantation (allo-HCT). GVHD often affects the intestine and is associated with a poor prognosis. Although frequently detectable, proinflammatory mechanisms exerted by intestinal tissue-infiltrating Th cell subsets remain to be fully elucidated. Here, we show that the Th17-defining transcription factor basic leucine zipper transcription factor ATF-like (BATF) was strongly regulated across human and mouse intestinal GVHD tissues. Studies in complete MHC-mismatched and minor histocompatibility-mismatched (miHA-mismatched) GVHD models revealed that BATF-expressing T cells were functionally indispensable for intestinal GVHD manifestation. Mechanistically, BATF controlled the formation of colon-infiltrating, IL-7 receptor-positive (IL-7R+), granulocyte-macrophage colony-stimulating factor-positive (GM-CSF+), donor T effector memory (Tem) cells. This T cell subset was sufficient to promote intestinal GVHD, while its occurrence was largely dependent on T cell-intrinsic BATF expression, required IL-7-IL-7R interaction, and was enhanced by GM-CSF. Thus, this study identifies BATF-dependent pathogenic GM-CSF+ effector T cells as critical promoters of intestinal inflammation in GVHD and hence putatively provides mechanistic insight into inflammatory processes previously assumed to be selectively Th17 driven.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1801
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:In-Data-Review

  5 / 18762 MEDLINE  
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[PMID]: 29274868
[Au] Autor:Zhao W; Ajani JA; Sushovan G; Ochi N; Hwang R; Hafley M; Johnson RL; Bresalier RS; Logsdon CD; Zhang Z; Song S
[Ad] Address:Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education) and Department of Cell Biology, Peking University Cancer Hospital and Institute, Beijing, People's Republic of China; Departments of Gastrointestinal Medical Oncology, University of Texas M.D. Anderson Cancer Center,
[Ti] Title:Galectin-3 Mediates Tumor Cell-Stroma Interactions by Activating Pancreatic Stellate Cells to Produce Cytokines via Integrin Signaling.
[So] Source:Gastroenterology;, 2017 Dec 21.
[Is] ISSN:1528-0012
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:BACKGROUND & AIMS: Pancreatic ductal adenocarcinoma (PDAC) is characterized by activated pancreatic stellate cells (PSCs), abundance of extracellular matrix (ECM), and production of cytokines and chemokines. Galectin 3 (GAL3), a ß-galactoside-specific lectin, contributes to PDAC development but its effects on the stroma and cytokine production are unclear. METHODS: The effect of recombinant human GAL3 (rGAL3) on activation of PSCs, production of cytokines, and ECM proteins was determined by proliferation, invasion, cytokine array, and quantitative polymerase chain reaction. We assessed co-cultures of PDAC cells with GAL3 genetic alterations with PSCs. Production of interleukin 8 (IL8) and activities of nuclear factor (NF)-κB were determined by enzyme-linked immunosorbent assay and luciferase reporter analyses. We studied the effects of inhibitors of NF-κB and integrin-linked kinase (ILK) on pathways activated by rGAL3. RESULTS: In analyses of the Gene Expression Omnibus database and our dataset, we observed higher levels of GAL3, IL8, and other cytokines in PDAC than in nontumor tissues. Production of IL8, granulocyte-macrophage colony-stimulating factor, chemokine ligand 1, and C-C motif chemokine ligand 2 increased in PSCs exposed to rGAL3 compared with controls. Culture of PSCs with PDAC cells that express different levels of GAL3 resulted in proliferation and invasion of PSCs that increased with level of GAL3. GAL3 stimulated transcription of IL8 through integrin subunit beta 1 (ITGB1) on PSCs, which activates NF-κB through ILK. Inhibitors of ILK or NF-κB or a neutralizing antibody against ITGB1 blocked transcription and production of IL8 from PSCs induced by rGAL3. The GAL3 inhibitor significantly reduced growth and metastases of orthotopic tumors that formed from PDAC and PSC cells co-implanted in mice. CONCLUSION: GAL3 activates PSC cells to produce inflammatory cytokines via ITGB1signaling to ILK and activation of NF-κB. Inhibition of this pathway reduced growth and metastases of pancreatic orthotopic tumors in mice.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1712
[Cu] Class update date: 180308
[Lr] Last revision date:180308
[St] Status:Publisher

  6 / 18762 MEDLINE  
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[PMID]: 29351125
[Au] Autor:Nicol LSC; Thornton P; Hatcher JP; Glover CP; Webster CI; Burrell M; Hammett K; Jones CA; Sleeman MA; Billinton A; Chessell I
[Ad] Address:Respiratory, Inflammation and Autoimmunity Research, MedImmune, Cambridge, United Kingdom.
[Ti] Title:Central inhibition of granulocyte-macrophage colony-stimulating factor is analgesic in experimental neuropathic pain.
[So] Source:Pain;159(3):550-559, 2018 Mar.
[Is] ISSN:1872-6623
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:With less than 50% of patients responding to the current standard of care and poor efficacy and selectivity of current treatments, neuropathic pain continues to be an area of considerable unmet medical need. Biological therapeutics such as monoclonal antibodies (mAbs) provide better intrinsic selectivity; however, delivery to the central nervous system (CNS) remains a challenge. Granulocyte-macrophage colony-stimulating factor (GM-CSF) is well described in inflammation-induced pain, and early-phase clinical trials evaluating its antagonism have exemplified its importance as a peripheral pain target. Here, we investigate the role of this cytokine in a murine model of traumatic nerve injury and show that deletion of the GM-CSF receptor or treatment with an antagonizing mAb alleviates pain. We also demonstrate enhanced analgesic efficacy using an engineered construct that has greater capacity to penetrate the CNS. Despite observing GM-CSF receptor expression in microglia and astrocytes, the gliosis response in the dorsal horn was not altered in nerve injured knockout mice compared with wild-type littermate controls as evaluated by ionized calcium binding adapter molecule 1 (Iba1) and glial fibrillary acidic protein, respectively. Functional analysis of glial cells revealed that pretreatment with GM-CSF potentiated lipopolysaccharide-induced release of proinflammatory cytokines. In summary, our data indicate that GM-CSF is a proinflammatory cytokine that contributes to nociceptive signalling through driving spinal glial cell secretion of proinflammatory mediators. In addition, we report a successful approach to accessing CNS pain targets, providing promise for central compartment delivery of analgesics.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1801
[Cu] Class update date: 180307
[Lr] Last revision date:180307
[St] Status:In-Data-Review
[do] DOI:10.1097/j.pain.0000000000001130

  7 / 18762 MEDLINE  
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[PMID]: 29235255
[Au] Autor:Bloch S; Zwicker S; Bostanci N; Sjöling Å; Boström EA; Belibasakis GN; Schäffer C
[Ad] Address:Department of NanoBiotechnology, NanoGlycobiology unit, Universität für Bodenkultur Wien, Vienna, Austria.
[Ti] Title:Immune response profiling of primary monocytes and oral keratinocytes to different Tannerella forsythia strains and their cell surface mutants.
[So] Source:Mol Oral Microbiol;33(2):155-167, 2018 Apr.
[Is] ISSN:2041-1014
[Cp] Country of publication:Denmark
[La] Language:eng
[Ab] Abstract:The oral pathogen Tannerella forsythia possesses a unique surface (S-) layer with a complex O-glycan containing a bacterial sialic acid mimic in the form of either pseudaminic acid or legionaminic acid at its terminal position. We hypothesize that different T. forsythia strains employ these stereoisomeric sugar acids for interacting with the immune system and resident host tissues in the periodontium. Here, we show how T. forsythia strains ATCC 43037 and UB4 displaying pseudaminic acid and legionaminic acid, respectively, and selected cell surface mutants of these strains modulate the immune response in monocytes and human oral keratinocytes (HOK) using a multiplex immunoassay. When challenged with T. forsythia, monocytes secrete proinflammatory cytokines, chemokines and vascular endothelial growth factor (VEGF) with the release of interleukin-1ß (IL-1ß) and IL-7 being differentially regulated by the two T. forsythia wild-type strains. Truncation of the bacteria's O-glycan leads to significant reduction of IL-1ß and regulates macrophage inflammatory protein-1. HOK infected with T. forsythia produce IL-1Ra, chemokines and VEGF. Although the two wild-type strains elicit preferential immune responses for IL-8, both truncation of the O-glycan and deletion of the S-layer result in significantly increased release of IL-8, granulocyte-macrophage colony-stimulating factor and monocyte chemoattractant protein-1. Through immunofluorescence and confocal laser scanning microscopy of infected HOK we additionally show that T. forsythia is highly invasive and tends to localize to the perinuclear region. This indicates, that the T. forsythia S-layer and attached sugars, particularly pseudaminic acid in ATCC 43037, contribute to dampening the response of epithelial tissues to initial infection and hence play a pivotal role in orchestrating the bacterium's virulence.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1712
[Cu] Class update date: 180306
[Lr] Last revision date:180306
[St] Status:In-Data-Review
[do] DOI:10.1111/omi.12208

  8 / 18762 MEDLINE  
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[PMID]: 29290406
[Au] Autor:Imitola J; Rasouli J; Watanabe F; Mahajan K; Sharan AD; Ciric B; Zhang GX; Rostami A
[Ad] Address:Department of Neurology, Division of Multiple Sclerosis and Neuroimmunology, Thomas Jefferson University, 900 Walnut Street, Suite 300, Philadelphia, PA 19107, USA; Division of Neuroimmunology and Multiple Sclerosis, The Ohio State University, OH, 43210, USA; Laboratory for Neural Stem Cells and Fun
[Ti] Title:Elevated expression of granulocyte-macrophage colony-stimulating factor receptor in multiple sclerosis lesions.
[So] Source:J Neuroimmunol;317:45-54, 2018 Apr 15.
[Is] ISSN:1872-8421
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:Multiple sclerosis (MS) is a chronic inflammatory demyelinating and neurodegenerative disease that disproportionately affects young adults, leading to disability and high costs to society. Infiltration of T cells and monocytes into the central nervous system (CNS) is critical for disease initiation and progression. However, despite a great deal of effort the molecular mechanisms by which immune cells initiate and perpetuate CNS damage in MS have not yet been elucidated. In experimental autoimmune encephalomyelitis (EAE), an animal model of MS, granulocyte-macrophage colony-stimulating factor (GM-CSF) produced by pathogenic Th1 and Th17 cells is critical for the recruitment of monocytes into the CNS during the initial stage of disease. We and others have recently shown that, compared with healthy individuals, MS patients have greater numbers of CD4 and CD8 T cells that produce GM-CSF. Here, we describe the expression of GM-CSF and its receptor, GM-CSFR, in normal brain and MS lesions. Our data show that in acute and chronic MS lesions, microglia and astrocytes have upregulated expression of GM-CSFR; in addition, we show that GM-CSF-associated molecules are also upregulated in MS lesions. These findings further strengthen the argument that GM-CSF signaling contributes to MS pathogenesis.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1801
[Cu] Class update date: 180304
[Lr] Last revision date:180304
[St] Status:In-Data-Review

  9 / 18762 MEDLINE  
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[PMID]: 29386427
[Au] Autor:Tachibana M
[Ad] Address:Laboratory of Biotechnology and Therapeutics, Graduate School of Pharmaceutical Sciences, Osaka University.
[Ti] Title:[The Immunosuppressive Function of Myeloid-derived Suppressor Cells Is Regulated by the HMGB1-TLR4 Axis].
[So] Source:Yakugaku Zasshi;138(2):143-148, 2018.
[Is] ISSN:1347-5231
[Cp] Country of publication:Japan
[La] Language:jpn
[Ab] Abstract: Myeloid-derived suppressor cells (MDSCs) accumulate under pathological conditions, including cancer and chronic inflammation, and they suppress various immune responses such as T cell proliferation. Although several inflammatory signals enhance the differentiation and/or function of MDSCs, it is not clear which factors regulate their differentiation and immunosuppressive function. It has been highlighted that damage-associated molecular patterns (DAMPs) play important roles in the induction of inflammation. One of the DAMPs, the high mobility group box 1 (HMGB1), is released from necrotic cells and secreted by macrophages. It has been shown that HMGB1 level is elevated in tumors and tumor-bearing hosts. It has also been reported that HMGB1 transduces intracellular signaling via several receptors, including the receptor for advanced glycation end-products (RAGE) and the toll-like receptor (TLR)4, both of which enhance the differentiation and/or function of MDSCs. However, the effects of HMGB1 on MDSCs remain unclear. In the present study, we examined the effect of HMGB1 on in vitro MDSC differentiation and immunosuppressive functions. Since murine bone marrow (BM) cells can differentiate into MDSCs upon granulocyte-macrophage colony-stimulating factor (GM-CSF) stimulation for 4 d in vitro, we cultured murine BM cells in the presence of HMGB1 and GM-CSF. The results demonstrated that HMGB1 enhanced the suppressive activity of in vitro MDSCs, depending on TLR4, whereas lipopolysaccharide (LPS), one of the TLR4 ligands, interfered with this differentiation and immunosuppressive activity of in vitro MDSCs, depending on TLR4. Our findings thus suggest that the HMGB1-TLR4 axis enhances the immunosuppressive function of MDSCs.
[Mh] MeSH terms primary: Bone Marrow Cells/immunology
HMGB1 Protein/physiology
Immunosuppression
Signal Transduction/physiology
Toll-Like Receptor 4/physiology
[Mh] MeSH terms secundary: Alarmins
Animals
Bone Marrow Cells/cytology
Cell Differentiation
Glycation End Products, Advanced
Humans
Inflammation/immunology
Mice
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Nm] Name of substance:0 (Alarmins); 0 (Glycation End Products, Advanced); 0 (HMGB1 Protein); 0 (Toll-Like Receptor 4)
[Em] Entry month:1802
[Cu] Class update date: 180228
[Lr] Last revision date:180228
[Js] Journal subset:IM
[Da] Date of entry for processing:180202
[St] Status:MEDLINE
[do] DOI:10.1248/yakushi.17-00158

  10 / 18762 MEDLINE  
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[PMID]: 29251350
[Au] Autor:Mosabbir AA; Qudrat A; Truong K
[Ad] Address:Institute of Biomaterials and Biomedical Engineering, University of Toronto, Toronto, Ontario, Canada.
[Ti] Title:Engineered cell migration to lesions linked to autoimmune disease.
[So] Source:Biotechnol Bioeng;115(4):1028-1036, 2018 Apr.
[Is] ISSN:1097-0290
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:The damaging and degenerative effects in autoimmune diseases such as rheumatoid arthritis, multiple sclerosis and Crohn's disease often manifests as the formation of lesions that feature a high local concentration of granulocyte-macrophage colony-stimulating factor (GM-CSF). GM-CSF along with other pro-inflammatory factors form a positive feedback loop that ultimately perpetuate the lesions. Hence, to engineer chemotaxis to GM-CSF, we created a new chimeric GM-CSF receptor alpha subunit (GMRchi) that was coupled with a previously engineered Ca -activated RhoA. When these proteins were expressed in mammalian cells, it allowed migration to chemical and cellular sources of GM-CSF. As a possible therapeutic intervention, we further implemented the mechanism of cell-cell membrane fusion and subsequent death. Since the microenvironment of lesions is more than just GM-CSF secretion, the further ability to recognize a combination of other features such as tissue markers will be needed for greater specificity. Nonetheless, this work represents a first step to enable cell-based therapy of autoimmune lesions.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1712
[Cu] Class update date: 180228
[Lr] Last revision date:180228
[St] Status:In-Data-Review
[do] DOI:10.1002/bit.26523


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