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PMID |
Sentence |
1 |
34925317
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Mechanistically, pretreatment with HPS effectively regulated macrophage polarization by shifting proinflammatory M1 macrophages (F4/80+CD11b+CD86+) to anti-inflammatory M2 ones (F4/80+CD11b+CD206+) in vivo and in bone marrow-derived macrophages (BMDMs) in vitro, resulting in the inhibition of renal proinflammatory macrophage infiltration and the reduction in expression of monocyte chemoattractant protein-1 (MCP-1), tumor necrosis factor (TNF-α) and inducible nitric oxide synthase (iNOS) while increasing expression of anti-inflammatory cytokine Arg-1 and CD163/CD206 surface molecules.
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2 |
34925317
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Unexpectedly, pretreatment with HPS suppressed CD4+ T cell proliferation in a coculture model of IL-4-induced M2 macrophages and splenic CD4+ T cells while promoting their differentiation into CD4+IL-4+ Th2 and CD4+Foxp3+ Treg cells.
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3 |
33571932
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No significant variation was observed in Th17 cell frequency, retinoic acid receptor-related orphan nuclear receptor γt (RORɣt), signal transducer and Activator of transcription 3(STAT3), IL-17, and IL-23, while IL-21, IL-4, and IL-10 had significant increase in mRNA expression and protein level of peripheral blood mononuclear cells in IMN cases.
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4 |
33571932
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Reduction in the percentage of Treg cells was also accompanied with significantly decreased expression of Forkhead box P3(FOXP3) and Transforming growth factor beta(TGF-β) in IMN patients compared to the control group.
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5 |
32961903
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Patients with T2D showed elevated IL-1Ra, IL-6, IL-17A, G-CSF, IP-10, MIP-1α, and bFGF levels; concentrations of IL-4, IL-12, IL-15, INF-γ, and VEGF were decreased.
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6 |
32961903
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IL-6, IL-17A, G-CSF, MIP-1α, and bFGF correlated negatively with eGFR; IL-10 and VEGF demonstrated negative associations with WFDC2; no relationships with podocyte markers were found.
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7 |
32961903
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Adjusted IL-17A and MIP-1α were predictors of non-albuminuric CKD, IL-13 predicted albuminuria with preserved renal function, meanwhile, IL-6 and hsCRP were predictors of albuminuria with eGFR decline.
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8 |
29093269
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Since IL-4 is a specific activator of STAT6, we analyzed kidney biopsies and demonstrated STAT6 activation in up to 1 of 3 of minimal change disease patients, suggesting IL-4 or IL-13 exposure in these patients.
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9 |
28871938
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Routine biochemical method was used to quantify 24-hour urine protein; the numbers of CD4+ and CD8+ T cells were detected by flow cytometry; the serum levels of interleukin 2 (IL-2), IL-4 and IL-17, the levels of urinary podocalyxin (PCX) and B7-1, the renal calcineurin (CaN) content were determined by ELISA.
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10 |
28871938
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Routine biochemical method was used to quantify 24-hour urine protein; the numbers of CD4+ and CD8+ T cells were detected by flow cytometry; the serum levels of interleukin 2 (IL-2), IL-4 and IL-17, the levels of urinary podocalyxin (PCX) and B7-1, the renal calcineurin (CaN) content were determined by ELISA.
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11 |
28871938
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Routine biochemical method was used to quantify 24-hour urine protein; the numbers of CD4+ and CD8+ T cells were detected by flow cytometry; the serum levels of interleukin 2 (IL-2), IL-4 and IL-17, the levels of urinary podocalyxin (PCX) and B7-1, the renal calcineurin (CaN) content were determined by ELISA.
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12 |
28871938
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Results Compared with the normal group, the levels of 24-hour urine protein, CD8+ T cells, serum IL-2 and IL-17, urinary PCX and B7-1, CaN in the model group were higher.
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13 |
28871938
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Results Compared with the normal group, the levels of 24-hour urine protein, CD8+ T cells, serum IL-2 and IL-17, urinary PCX and B7-1, CaN in the model group were higher.
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14 |
28871938
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Results Compared with the normal group, the levels of 24-hour urine protein, CD8+ T cells, serum IL-2 and IL-17, urinary PCX and B7-1, CaN in the model group were higher.
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15 |
28871938
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The whole blood CD4+ T cell number and serum IL-4 level in the model group were lower than those in the normal group, they were higher in the valsartan group and control group than in the model group.
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16 |
28871938
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The whole blood CD4+ T cell number and serum IL-4 level in the model group were lower than those in the normal group, they were higher in the valsartan group and control group than in the model group.
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17 |
28871938
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The whole blood CD4+ T cell number and serum IL-4 level in the model group were lower than those in the normal group, they were higher in the valsartan group and control group than in the model group.
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18 |
28871938
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The mechanism may be related to the regulation of CD4+ T and CD8+ T cell numbers, the down-regulated expressions of serum IL-2, IL-17, the decreased levels of PCX and B7-1 in urine, CaN in kidney tissue, and the up-regulated level of serum IL-4.
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19 |
28871938
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The mechanism may be related to the regulation of CD4+ T and CD8+ T cell numbers, the down-regulated expressions of serum IL-2, IL-17, the decreased levels of PCX and B7-1 in urine, CaN in kidney tissue, and the up-regulated level of serum IL-4.
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20 |
28871938
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The mechanism may be related to the regulation of CD4+ T and CD8+ T cell numbers, the down-regulated expressions of serum IL-2, IL-17, the decreased levels of PCX and B7-1 in urine, CaN in kidney tissue, and the up-regulated level of serum IL-4.
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21 |
27815317
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Cultured macrophages with COX-2 deletion exhibited an M1 phenotype, as demonstrated by higher inducible nitric oxide synthase and nuclear factor-κB levels but lower interleukin-4 receptor-α levels.
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22 |
27160965
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Moreover, retinoids were also shown to affect the synthesis of different cytokines specific both for lymphocytes Th1 (IL-2, IL-12, INFγ) ant Th2 (IL-4, IL-10).
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23 |
26988026
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In addition, BMCs co-treatment decreased the extent of neutrophil infiltration and modulated the inflammatory response by shifting from pro-inflammatory Th1 to an anti-inflammatory Th2 profile, where IL-1β, TNF-α, IL-6 and IFN-γ levels declined and IL-10 and IL-4 levels increased.
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24 |
26440060
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Dendritic cell-specific intercellular adhesion molecule-3-grabbing non-integrin (DC-SIGN) is an innate immune molecular that has an immune recognition function, and is involved in mediation of cell adhesion and immunoregulation.
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25 |
26440060
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DC-SIGN was co-expressed with nephrin on podocytes.
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26 |
26440060
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After the podocytes were stimulated by serum of LN mice in vitro, the expression of DC-SIGN, major histocompatibility complex (MHC) class II and CD80 was up-regulated, stimulation of T cell proliferation was enhanced and the interferon (IFN)-γ/interleukin (IL)-4 ratio increased.
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27 |
25904903
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NKT cell-associated cytokines such as IL-2, IL-4, IFN-γ, and IL-17 were detected in kidney lysates of Stx2-injected WT mice with the peak around 36 h after Stx2 injection.
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28 |
25173645
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Renal remodeling, function, ER stress (CHOP and GRP78) and inflammation (infiltration of inflammatory cells, NF-κB p65) were evaluated 12 weeks after MI.
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29 |
25173645
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However, MI significantly increased the glomerular expression of GRP78 and CHOP in UNX and DB rats.
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30 |
25173645
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In addition, it also promoted the infiltration of CD4+ T cells, particularly inflammatory cytokine (IFN-γ, IL-17, IL-4)-producing CD4+ T cells, and the expression of NF-κB p65 in the glomeruli.
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31 |
22427838
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Using an adriamycin(ADM)-based model of FSGS, we found that BALB/c mice presented albuminuria and glomerular degeneration in association with a Th2-like pro-fibrogenic profile; these mice also expressed a combination of inflammatory cytokines, such as IL-4, IL-1α, IL-1β, IL-17, TNF-α, and chemokines, such as RANTES and eotaxin.
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32 |
22427838
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TGF-β analysis revealed increased levels of circulating protein and tissue transcripts in both ADM- and GSL-1-treated mice, suggesting that TGF-β could be associated with both FSGS pathology and iNKT-mediated immunosuppression; therefore, we analyzed the kidney expression of phosphorylated SMAD2/3 and SMAD7 proteins, molecules associated with the deleterious and protective effects of TGF-β, respectively.
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33 |
7586682
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Interferon-gamma (IFN-gamma) and IL-4 expressed during mercury-induced membranous nephropathy are toxic for cultured podocytes.
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34 |
7586682
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Interferon-gamma (IFN-gamma) and IL-4 expressed during mercury-induced membranous nephropathy are toxic for cultured podocytes.
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35 |
7586682
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Interferon-gamma (IFN-gamma) and IL-4 expressed during mercury-induced membranous nephropathy are toxic for cultured podocytes.
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36 |
7586682
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Interferon-gamma (IFN-gamma) and IL-4 expressed during mercury-induced membranous nephropathy are toxic for cultured podocytes.
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37 |
7586682
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Interferon-gamma (IFN-gamma) and IL-4 expressed during mercury-induced membranous nephropathy are toxic for cultured podocytes.
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38 |
7586682
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Interferon-gamma (IFN-gamma) and IL-4 expressed during mercury-induced membranous nephropathy are toxic for cultured podocytes.
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39 |
7586682
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In diseased rats a five-fold increase in intraglomerular macrophages was found, but we could not detect intraglomerular IFN-alpha, IFN-beta, IL-1 beta or tumour necrosis factor-alpha (TNF-alpha) by using immunohistology.
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40 |
7586682
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In diseased rats a five-fold increase in intraglomerular macrophages was found, but we could not detect intraglomerular IFN-alpha, IFN-beta, IL-1 beta or tumour necrosis factor-alpha (TNF-alpha) by using immunohistology.
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41 |
7586682
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In diseased rats a five-fold increase in intraglomerular macrophages was found, but we could not detect intraglomerular IFN-alpha, IFN-beta, IL-1 beta or tumour necrosis factor-alpha (TNF-alpha) by using immunohistology.
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42 |
7586682
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In diseased rats a five-fold increase in intraglomerular macrophages was found, but we could not detect intraglomerular IFN-alpha, IFN-beta, IL-1 beta or tumour necrosis factor-alpha (TNF-alpha) by using immunohistology.
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43 |
7586682
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In diseased rats a five-fold increase in intraglomerular macrophages was found, but we could not detect intraglomerular IFN-alpha, IFN-beta, IL-1 beta or tumour necrosis factor-alpha (TNF-alpha) by using immunohistology.
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44 |
7586682
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In diseased rats a five-fold increase in intraglomerular macrophages was found, but we could not detect intraglomerular IFN-alpha, IFN-beta, IL-1 beta or tumour necrosis factor-alpha (TNF-alpha) by using immunohistology.
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45 |
7586682
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IFN-gamma and IL-4 were the only cytokines that exerted toxic effects, resulting in a rapidly decreased transepithelial resistance of confluent monolayers, which was closely associated with altered immunoreactivity of the tight junction protein ZO-1.
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46 |
7586682
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IFN-gamma and IL-4 were the only cytokines that exerted toxic effects, resulting in a rapidly decreased transepithelial resistance of confluent monolayers, which was closely associated with altered immunoreactivity of the tight junction protein ZO-1.
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47 |
7586682
|
IFN-gamma and IL-4 were the only cytokines that exerted toxic effects, resulting in a rapidly decreased transepithelial resistance of confluent monolayers, which was closely associated with altered immunoreactivity of the tight junction protein ZO-1.
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48 |
7586682
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IFN-gamma and IL-4 were the only cytokines that exerted toxic effects, resulting in a rapidly decreased transepithelial resistance of confluent monolayers, which was closely associated with altered immunoreactivity of the tight junction protein ZO-1.
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49 |
7586682
|
IFN-gamma and IL-4 were the only cytokines that exerted toxic effects, resulting in a rapidly decreased transepithelial resistance of confluent monolayers, which was closely associated with altered immunoreactivity of the tight junction protein ZO-1.
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50 |
7586682
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IFN-gamma and IL-4 were the only cytokines that exerted toxic effects, resulting in a rapidly decreased transepithelial resistance of confluent monolayers, which was closely associated with altered immunoreactivity of the tight junction protein ZO-1.
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51 |
7586682
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IL-4 also affected vimentin and laminin immunoreactivity.
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52 |
7586682
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IL-4 also affected vimentin and laminin immunoreactivity.
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53 |
7586682
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IL-4 also affected vimentin and laminin immunoreactivity.
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54 |
7586682
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IL-4 also affected vimentin and laminin immunoreactivity.
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55 |
7586682
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IL-4 also affected vimentin and laminin immunoreactivity.
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56 |
7586682
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IL-4 also affected vimentin and laminin immunoreactivity.
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57 |
7586682
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IFN-gamma and IL-4 only interfered with monolayer integrity when added to the basolateral side of the GVEC, indicating specific (receptor-mediated) effects.
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58 |
7586682
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IFN-gamma and IL-4 only interfered with monolayer integrity when added to the basolateral side of the GVEC, indicating specific (receptor-mediated) effects.
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59 |
7586682
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IFN-gamma and IL-4 only interfered with monolayer integrity when added to the basolateral side of the GVEC, indicating specific (receptor-mediated) effects.
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60 |
7586682
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IFN-gamma and IL-4 only interfered with monolayer integrity when added to the basolateral side of the GVEC, indicating specific (receptor-mediated) effects.
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61 |
7586682
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IFN-gamma and IL-4 only interfered with monolayer integrity when added to the basolateral side of the GVEC, indicating specific (receptor-mediated) effects.
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62 |
7586682
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IFN-gamma and IL-4 only interfered with monolayer integrity when added to the basolateral side of the GVEC, indicating specific (receptor-mediated) effects.
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63 |
7586682
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From our experiments we concluded that IFN-gamma subtly affected monolayer integrity at the level of the tight junctions, and that IL-4 additionally induced cell death.
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64 |
7586682
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From our experiments we concluded that IFN-gamma subtly affected monolayer integrity at the level of the tight junctions, and that IL-4 additionally induced cell death.
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65 |
7586682
|
From our experiments we concluded that IFN-gamma subtly affected monolayer integrity at the level of the tight junctions, and that IL-4 additionally induced cell death.
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66 |
7586682
|
From our experiments we concluded that IFN-gamma subtly affected monolayer integrity at the level of the tight junctions, and that IL-4 additionally induced cell death.
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67 |
7586682
|
From our experiments we concluded that IFN-gamma subtly affected monolayer integrity at the level of the tight junctions, and that IL-4 additionally induced cell death.
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68 |
7586682
|
From our experiments we concluded that IFN-gamma subtly affected monolayer integrity at the level of the tight junctions, and that IL-4 additionally induced cell death.
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69 |
7586682
|
We hypothesize that the toxic effects of the cytokines IFN-gamma and IL-4 as seen with cultured podocytes are necessary together with the autoantibodies, for the ultimate induction of proteinuria in mercury nephropathy in the DZB rat.
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70 |
7586682
|
We hypothesize that the toxic effects of the cytokines IFN-gamma and IL-4 as seen with cultured podocytes are necessary together with the autoantibodies, for the ultimate induction of proteinuria in mercury nephropathy in the DZB rat.
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71 |
7586682
|
We hypothesize that the toxic effects of the cytokines IFN-gamma and IL-4 as seen with cultured podocytes are necessary together with the autoantibodies, for the ultimate induction of proteinuria in mercury nephropathy in the DZB rat.
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72 |
7586682
|
We hypothesize that the toxic effects of the cytokines IFN-gamma and IL-4 as seen with cultured podocytes are necessary together with the autoantibodies, for the ultimate induction of proteinuria in mercury nephropathy in the DZB rat.
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73 |
7586682
|
We hypothesize that the toxic effects of the cytokines IFN-gamma and IL-4 as seen with cultured podocytes are necessary together with the autoantibodies, for the ultimate induction of proteinuria in mercury nephropathy in the DZB rat.
|
74 |
7586682
|
We hypothesize that the toxic effects of the cytokines IFN-gamma and IL-4 as seen with cultured podocytes are necessary together with the autoantibodies, for the ultimate induction of proteinuria in mercury nephropathy in the DZB rat.
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