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PMID |
Sentence |
1 |
8093442
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Association of tumor necrosis factor (TNF) and class II major histocompatibility complex alleles with the secretion of TNF-alpha and TNF-beta by human mononuclear cells: a possible link to insulin-dependent diabetes mellitus.
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2 |
8093442
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We have investigated the correlation between different tumor necrosis factor (TNF) and class II major histocompatibility complex alleles in the lipopolysaccharide- or phytohemagglutinin-induced secretion of TNF-alpha and TNF-beta by human monocytes and peripheral blood mononuclear cells in 87 unrelated Danish male individuals.
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3 |
8093442
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Significant differences in TNF-alpha secretory capacity between TNF NcoI restriction fragment length polymorphisms, TNFa and TNFc microsatellite alleles and DR alleles were identified.
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4 |
8093442
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In a group of DR3/DR4 heterozygous patients with insulin-dependent diabetes mellitus (IDDM), the frequency of the TNFa2 allele was higher than in HLA-DR matched controls, whereas the TNFa6 allele was more frequent in control individuals.
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5 |
8093442
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In the DR3/DR4 heterozygous diabetic group 12/26 had the alleles combination DQw8, DR4 (Dw4), C4A3, TNFB*2, TNFa2, B15, whereas only 1/18 controls had this haplotype.
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6 |
8093442
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This diabetogenic haplotype is identical to the DR4 haplotype which correlates with a higher TNF-alpha response.
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7 |
8093442
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These observations suggest a direct role for the TNF locus in the pathogenesis of IDDM.
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8 |
8898563
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Specific substrates of the ADP-ribosyltransferases have been identified; the skeletal muscle transferase ADP-ribosylates integrin alpha 7 whereas the chicken heterophil enzyme modifies the heterophil granule protein p33 and the CTL enzyme ADP-ribosylates the membrane-associated protein p40.
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9 |
11390440
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To explore the potential role of LT-mediated microenvironment in the pathogenesis of insulin-dependent diabetes mellitus (IDDM), an LTbeta receptor-immunoglobulin fusion protein (LTbetaR-Ig) was administered to nonobese diabetic mice.
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10 |
11390441
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A critical role for lymphotoxin-beta receptor in the development of diabetes in nonobese diabetic mice.
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11 |
11390441
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To assess the role of lymphotoxin-beta receptor (LTbetaR) in diabetes pathogenesis, we expressed an LTbetaR-Fc fusion protein in nonobese diabetic (NOD) mice.
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12 |
11390441
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A critical role for lymphotoxin-beta receptor in the development of diabetes in nonobese diabetic mice.
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13 |
11390441
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To assess the role of lymphotoxin-beta receptor (LTbetaR) in diabetes pathogenesis, we expressed an LTbetaR-Fc fusion protein in nonobese diabetic (NOD) mice.
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14 |
11857053
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A family-based study was carried out in 67 Bangladeshi families, consisting of a proband with FCPD and both parents, to determine whether an association exists between FCPD susceptibility and either the major histocompatiblity complex (MHC) or insulin gene (INS) loci.
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15 |
11857053
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HLA-DQB1 typing was done using allele-specific primers, and INS was typed using the restriction enzyme HphI.
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16 |
11857053
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Three microsatellites (TNFa, TNFc and TNFd), from within and flanking the TNF-LT locus, were used for MHC Class IV typing and a PCR-RFLP assay was used to define the -308G/A TNF promoter polymorphism.
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17 |
11857053
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This study confirms an association between FCPD and the MHC using a family-based study design and the stringent ETDT analysis; a novel protective association was found with HLA-DQB1*0202 in Bangladeshi FCPD subjects.
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18 |
12058258
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In addition to the promoter polymorphism, TNFa and TNFc microsatellite genotypes were determined but these polymorphisms were not associated with morbidity or mortality.
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19 |
15561941
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Absence of lymph nodes in NOD mice treated with lymphotoxin-beta receptor immunoglobulin protects from diabetes.
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20 |
15561941
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Pregnant nonobese diabetic (NOD) mice were treated with lymphotoxin-beta receptor immunoglobulin fusion protein (LTbetaR-Ig) or control human immunoglobulin on days embryonic day 11 (E11) and E14, and offspring were followed for the development of anti-beta-cell antibodies, islet pathology, and hyperglycemia.
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21 |
15561941
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Absence of lymph nodes in NOD mice treated with lymphotoxin-beta receptor immunoglobulin protects from diabetes.
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22 |
15561941
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Pregnant nonobese diabetic (NOD) mice were treated with lymphotoxin-beta receptor immunoglobulin fusion protein (LTbetaR-Ig) or control human immunoglobulin on days embryonic day 11 (E11) and E14, and offspring were followed for the development of anti-beta-cell antibodies, islet pathology, and hyperglycemia.
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23 |
16367949
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Using quantitative reverse transcription-polymerase chain reaction (qRT-PCR) we studied the expression levels of interleukin (IL)-2, IL-4, IL-10, IL-12, IL-15, interferon (IFN)-gamma and tumour necrosis factor (TNF)-alpha during the course of LTB and SPTB in the lungs and spleens of B6D2F1Bom mice infected with the H37Rv strain of Mycobacterium tuberculosis (Mtb).
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24 |
16367949
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The results show that, except for IL-4, cytokine expression levels were significantly higher during SPTB than LTB in both the lungs and spleens.
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25 |
16367949
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During LTB, all the cytokines (except IL-2 in the lungs) had higher expression levels during the initial period of infection both in the lungs and spleens.
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26 |
16367949
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The expression levels of IL-10, IL-12 and IFN-gamma increased significantly from 2 to 3 in the lungs.
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27 |
16367949
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IL-10 and IL-15 increased significantly from phases 2 to 3, whereas that of TNF-alpha decreased significantly and progressively from phases 1 to 3 in the spleens.
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28 |
16367949
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In the present study, there was a progressive and significant increase in the expression levels of IL-15, together with Th1 cytokines (IL-12 and IFN-gamma) during SPTB but a significant decrease during LTB.
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29 |
16367949
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IL-15 is known to up-regulate the production of proinflammatory cytokines, IL-1beta, IL-8, IL-12, IL-17, IFN-gamma and TNF-alpha and has an inhibitory effect on activation-induced cell death.
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30 |
16367949
|
Using quantitative reverse transcription-polymerase chain reaction (qRT-PCR) we studied the expression levels of interleukin (IL)-2, IL-4, IL-10, IL-12, IL-15, interferon (IFN)-gamma and tumour necrosis factor (TNF)-alpha during the course of LTB and SPTB in the lungs and spleens of B6D2F1Bom mice infected with the H37Rv strain of Mycobacterium tuberculosis (Mtb).
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31 |
16367949
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The results show that, except for IL-4, cytokine expression levels were significantly higher during SPTB than LTB in both the lungs and spleens.
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32 |
16367949
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During LTB, all the cytokines (except IL-2 in the lungs) had higher expression levels during the initial period of infection both in the lungs and spleens.
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33 |
16367949
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The expression levels of IL-10, IL-12 and IFN-gamma increased significantly from 2 to 3 in the lungs.
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34 |
16367949
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IL-10 and IL-15 increased significantly from phases 2 to 3, whereas that of TNF-alpha decreased significantly and progressively from phases 1 to 3 in the spleens.
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35 |
16367949
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In the present study, there was a progressive and significant increase in the expression levels of IL-15, together with Th1 cytokines (IL-12 and IFN-gamma) during SPTB but a significant decrease during LTB.
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36 |
16367949
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IL-15 is known to up-regulate the production of proinflammatory cytokines, IL-1beta, IL-8, IL-12, IL-17, IFN-gamma and TNF-alpha and has an inhibitory effect on activation-induced cell death.
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37 |
16367949
|
Using quantitative reverse transcription-polymerase chain reaction (qRT-PCR) we studied the expression levels of interleukin (IL)-2, IL-4, IL-10, IL-12, IL-15, interferon (IFN)-gamma and tumour necrosis factor (TNF)-alpha during the course of LTB and SPTB in the lungs and spleens of B6D2F1Bom mice infected with the H37Rv strain of Mycobacterium tuberculosis (Mtb).
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38 |
16367949
|
The results show that, except for IL-4, cytokine expression levels were significantly higher during SPTB than LTB in both the lungs and spleens.
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39 |
16367949
|
During LTB, all the cytokines (except IL-2 in the lungs) had higher expression levels during the initial period of infection both in the lungs and spleens.
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40 |
16367949
|
The expression levels of IL-10, IL-12 and IFN-gamma increased significantly from 2 to 3 in the lungs.
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41 |
16367949
|
IL-10 and IL-15 increased significantly from phases 2 to 3, whereas that of TNF-alpha decreased significantly and progressively from phases 1 to 3 in the spleens.
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42 |
16367949
|
In the present study, there was a progressive and significant increase in the expression levels of IL-15, together with Th1 cytokines (IL-12 and IFN-gamma) during SPTB but a significant decrease during LTB.
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43 |
16367949
|
IL-15 is known to up-regulate the production of proinflammatory cytokines, IL-1beta, IL-8, IL-12, IL-17, IFN-gamma and TNF-alpha and has an inhibitory effect on activation-induced cell death.
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44 |
16367949
|
Using quantitative reverse transcription-polymerase chain reaction (qRT-PCR) we studied the expression levels of interleukin (IL)-2, IL-4, IL-10, IL-12, IL-15, interferon (IFN)-gamma and tumour necrosis factor (TNF)-alpha during the course of LTB and SPTB in the lungs and spleens of B6D2F1Bom mice infected with the H37Rv strain of Mycobacterium tuberculosis (Mtb).
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45 |
16367949
|
The results show that, except for IL-4, cytokine expression levels were significantly higher during SPTB than LTB in both the lungs and spleens.
|
46 |
16367949
|
During LTB, all the cytokines (except IL-2 in the lungs) had higher expression levels during the initial period of infection both in the lungs and spleens.
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47 |
16367949
|
The expression levels of IL-10, IL-12 and IFN-gamma increased significantly from 2 to 3 in the lungs.
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48 |
16367949
|
IL-10 and IL-15 increased significantly from phases 2 to 3, whereas that of TNF-alpha decreased significantly and progressively from phases 1 to 3 in the spleens.
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49 |
16367949
|
In the present study, there was a progressive and significant increase in the expression levels of IL-15, together with Th1 cytokines (IL-12 and IFN-gamma) during SPTB but a significant decrease during LTB.
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50 |
16367949
|
IL-15 is known to up-regulate the production of proinflammatory cytokines, IL-1beta, IL-8, IL-12, IL-17, IFN-gamma and TNF-alpha and has an inhibitory effect on activation-induced cell death.
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51 |
18417641
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Overall, these data support a novel role of PPARalpha as a regulator of lipid metabolism in the feto-placental unit, relevant in maternal diabetes where fetal and placental PPARalpha, LTB(4) and lipid concentrations are altered.
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