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PMID |
Sentence |
1 |
9536430
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Thus, a subset of both T cell and mAb allodeterminants are influenced by a DM-dependent interaction of MHC molecules with peptides, while the formation of DM-independent allodeterminants may represent direct MHC epitope recognition by the T cell receptor or an alternative peptide loading mechanism distinct from the HLA-DM pathways.
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2 |
10051633
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In addition to causing abnormal MHC expression, the ds nucleic acids increase the expression of genes necessary for antigen processing and presentation: proteasome proteins (e.g., LMP2), transporters of antigen peptides; invariant chain, HLA-DM, and the costimulatory molecule B7.1.
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3 |
10051633
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The ds nucleic acids also induce or activate Stat1, Stat3, mitogen-activated protein kinase, NF-kappaB, the class II transactivator, RFX5, and the IFN regulatory factor 1 differently from gammaIFN.
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4 |
10427471
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Implication of HLA-DMA alleles in corsican IDDM.
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5 |
10427471
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The study of the DMA gene could therefore be an additional tool for early IDDM diagnosis in the Corsican population.
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6 |
10427471
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Implication of HLA-DMA alleles in corsican IDDM.
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7 |
10427471
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The study of the DMA gene could therefore be an additional tool for early IDDM diagnosis in the Corsican population.
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8 |
10519369
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HLA-DMA and HLA-DMB alleles in German patients with type 1 diabetes mellitus.
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9 |
10519369
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The HLA-DMA and HLA-DMB genes are located in the HLA-D region between DQ and DP.
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10 |
10519369
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HLA-DMA and HLA-DMB alleles in German patients with type 1 diabetes mellitus.
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11 |
10519369
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The HLA-DMA and HLA-DMB genes are located in the HLA-D region between DQ and DP.
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12 |
11129119
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These include increased expression of proteasome processing proteins (LMP2), transporters of antigen peptides (TAP), invariant chain (Ii), HLA-DM, and the co-stimulatory molecule, B7, as well as STAT and NF-kappaB activation.
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13 |
11129119
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A critical factor in these changes is the loss of normal negative regulation of MHC class I, class II, and thyrotropin receptor (TSHR) gene expression, which is necessary to maintain self-tolerance during the normal changes in gene expression involved in hormonally-increased growth and function of the cell.
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14 |
11129119
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Self-tolerance to the TSHR is maintained in normals because there is a population of CD8- cells which normally suppresses a population of CD4+ cells that can interact with the TSHR if thyrocytes become APCs.
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15 |
21510113
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Proposed biological mechanisms in experimental animals included up regulation of inflammatory signals like cytokines and TNF-alpha, oxidative stress, hypomethylation, decreased DNA repair and apoptosis, cell proliferation, angiogenesis, activation of several enzymes like methyl transferase which converts inorganic arsenic to MMA and DMA, and GSH in in-vivo and in-vitro in experimental rat liver slices.
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16 |
21775680
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HLA-DM (DM) catalyzes CLIP release, stabilizes MHC class II molecules, and edits the peptide repertoire presented by class II.
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17 |
21775680
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The effects of mutations were investigated by measuring the peptide dissociation and exchange rate in vitro, CLIP and DQ2 expression on the cell surface, and the presentation of α-II-gliadin epitope (residues 62-70) to murine, DQ2-restricted T cell hybridomas.
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18 |
23434766
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We found that DMA inhibited inflammatory cytokine production via upregulation of nuclear factor-erythroid 2-related factor 2 (Nrf2) and alleviated oxidative stress through attenuation of p47phox translocation to the membrane of S100b-treated THP-1 monocytes.
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19 |
23434766
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We found that DMA activated Nrf2 mediated by the p38 kinase pathway in THP-1 monocytes.
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20 |
23434766
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The in vivo verification of anti-inflammation in peripheral blood mononuclear cells by DMA treatment was confirmed by tumor necrosis factor-α and interleukin-1β measurements.
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