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PMID |
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1 |
15185348
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Modulation by factors that affect T-cell function or hematopoiesis, including interleukin-12, interleukin-15, interleukin-18, interleukin-23, Eta-1, Flt3L and GM-CSF, was studied in the forms of monocistronic and bicistronic plasmid.
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2 |
15185348
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Our results demonstrated that vaccination of pHM could induce successful antitumor immunity against Her-2/neu-expressing murine tumor cells in BALB/c mice.
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3 |
15185348
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In particular, coexpression of interleukin-18 or GM-CSF with Her-2/neu increased antitumor activity in both preventive and therapeutic experiments.
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4 |
16988256
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Because it is known that SOCS are induced by IL-10 and that B. burgdorferi and its lipoproteins most likely interact via TLR2 or the heterodimers TLR2/1 and/or TLR2/6, we hypothesized that SOCS are induced by IL-10 and B. burgdorferi and its lipoproteins in macrophages and that SOCS may mediate the inhibition by IL-10 of concomitantly elicited cytokines.
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5 |
16988256
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We report here that mouse J774 macrophages incubated with IL-10 and added B. burgdorferi spirochetes (freeze-thawed, live, or sonicated) or lipidated outer surface protein A (L-OspA) augmented their SOCS1/SOCS3 mRNA and protein expression, with SOCS3 being more abundant.
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6 |
16988256
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Pam(3)Cys, a synthetic lipopeptide, also induced SOCS1/SOCS3 expression under these conditions, but unlipidated OspA was ineffective.
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7 |
16988256
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Neither endogenous IL-10 nor the translation inhibitor cycloheximide blocked SOCS1/SOCS3 induction by B. burgdorferi and its lipoproteins, indicating that the expression of other genes is not required.
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8 |
16988256
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This temporally correlated with the IL-10-mediated inhibition of the inflammatory cytokines IL-1beta, IL-6, IL-12p40, IL-18, and tumor necrosis factor alpha.
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9 |
16988256
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Our data are evidence to suggest that expression of SOCS is part of the mechanism of IL-10-mediated inhibition of inflammatory cytokines elicited by B. burgdorferi and its lipoproteins.
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10 |
19027958
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Chirality of TLR-2 ligand Pam3CysSK4 in fully synthetic peptide conjugates critically influences the induction of specific CD8+ T-cells.
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11 |
19027958
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In the current study we have investigated the behaviour of two diastereomers of the TLR-2 ligand Pam(3)CSK(4) (Pam) derivatives, namely the R- and S-epimers at C-2 of the glycerol moiety.
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12 |
19027958
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In summary we show that the favourable effects of the Pam(R)-configuration of TLR-2 ligand can be attributed to direct effects on dendritic cells resulting in enhancement of CD8(+) T-cell responses.
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13 |
19027958
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Chirality of TLR-2 ligand Pam3CysSK4 in fully synthetic peptide conjugates critically influences the induction of specific CD8+ T-cells.
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14 |
19027958
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In the current study we have investigated the behaviour of two diastereomers of the TLR-2 ligand Pam(3)CSK(4) (Pam) derivatives, namely the R- and S-epimers at C-2 of the glycerol moiety.
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15 |
19027958
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In summary we show that the favourable effects of the Pam(R)-configuration of TLR-2 ligand can be attributed to direct effects on dendritic cells resulting in enhancement of CD8(+) T-cell responses.
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16 |
19109135
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Activated human neonatal CD8+ T cells are subject to immunomodulation by direct TLR2 or TLR5 stimulation.
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17 |
19109135
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In concert with TCR stimulation, only Pam(3)Cys (palmitoyl-3-Cys-Ser-(Lys)(4)) and flagellin monomers significantly enhanced proliferation, CD25(+) expression, IL-2, IFN-gamma, TNF-alpha, and intracellular granzyme B expression.
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18 |
19109135
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TLR2 and TLR5 mRNA was detected in the CD8(+) T cells.
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19 |
19109135
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Blocking studies confirmed that the increase in IFN-gamma production was by the direct triggering of surface TLR2 or TLR5.
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20 |
19109135
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The simultaneous exposure of CD8(+) T cells to both TLR agonists had an additive effect on IFN-gamma production.
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21 |
19273561
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These two beta-glucans failed to stimulate TNF-alpha in Dectin-1 (beta-glucan receptor) knockout BMDCs.
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22 |
19273561
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The upregulation of TNF-alpha and downregulation of IL-12p70 required Dectin-1, but not IL-10.
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23 |
19273561
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Finally, costimulation of BMDCs with YGPs and either the TLR9 ligand, CpG, or the TLR2/1 ligand, Pam(3)CSK(4), resulted in upregulated secretion of IL-1alpha and IL-10 and downregulated secretion of IL-1beta, IL-6, and IFN-gamma-inducible protein 10 but had no significant effects on IL-12p40, keratinocyte-derived chemokine, monocyte chemotactic protein 1, or macrophage inflammatory protein alpha, compared with the TLR ligand alone.
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24 |
19694614
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Toll-like receptor-2 (TLR-2) agonist, Pam(3)Cys, was synthesized and coupled to CM-TMC through a polyethylene glycol (PEG) spacer.
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25 |
19694614
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In vitro studies using phorbol 12-myristyl 13-acetate (PMA) stimulated macrophage-like THP-1 (mTHP-1) cells were focused on cytotoxicity of both polymers and particles, and their potential to stimulate IL-8 release via the TLR-2 pathway.
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26 |
20445007
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The current studies used the Toll-like receptor 2 (TLR2) agonist palmitoyl(3)-cysteine-serine-lysine(4) (PAM) or the TLR4 agonist lipopolysaccharide (LPS) to stimulate human whole blood and determine whether postponing the addition of the GC dexamethasone (DEX) limits its ability to decrease cytokine production.
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27 |
20445007
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Twenty-four hours after stimulation, tumor necrosis factor (TNF), interleukin-1beta (IL-1beta), IL-6, and IL-8 levels were measured, in addition to the cytokine inhibitors IL-1 soluble receptor II (SRII), IL-1 receptor antagonist, and TNF SRII.
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28 |
20445007
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PAM stimulation also induced IL-1beta, IL-6, and IL-8.
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29 |
20445007
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Delaying the addition of DEX until 6 h after LPS stimulation failed to decrease TNF or IL-6.
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30 |
20445007
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In contrast, delayed DEX addition significantly suppressed PAM-induced IL-1beta, IL-6, or IL-8 and also suppressed LPS-induced IL-1beta and IL-8.
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31 |
20445007
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The current studies used the Toll-like receptor 2 (TLR2) agonist palmitoyl(3)-cysteine-serine-lysine(4) (PAM) or the TLR4 agonist lipopolysaccharide (LPS) to stimulate human whole blood and determine whether postponing the addition of the GC dexamethasone (DEX) limits its ability to decrease cytokine production.
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32 |
20445007
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Twenty-four hours after stimulation, tumor necrosis factor (TNF), interleukin-1beta (IL-1beta), IL-6, and IL-8 levels were measured, in addition to the cytokine inhibitors IL-1 soluble receptor II (SRII), IL-1 receptor antagonist, and TNF SRII.
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33 |
20445007
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PAM stimulation also induced IL-1beta, IL-6, and IL-8.
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34 |
20445007
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Delaying the addition of DEX until 6 h after LPS stimulation failed to decrease TNF or IL-6.
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35 |
20445007
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In contrast, delayed DEX addition significantly suppressed PAM-induced IL-1beta, IL-6, or IL-8 and also suppressed LPS-induced IL-1beta and IL-8.
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36 |
21056473
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In this study we investigate the feasibility of generating self-adjuvanting vaccines capable of inducing high titre antibody responses following the covalent attachment of the TLR2 agonist Pam(2)Cys to intact proteins.
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37 |
24534144
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Endosomal TLRs, TLR3, TLR7/8, and TLR9 are involved in antiviral responses by promoting the production of antiviral cytokines such as type I interferons.
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38 |
24534144
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The aim of the present study was to evaluate the expression of TLR3, TLR7 and TLR9 in porcine alveolar macrophages (PAM) infected with different genotype 1 PRRSV strains previously sequenced and characterized by their ability to induce TNF-α: 3262 (TNF-α inducer), 3267 (TNF-α not inducer) and an attenuated vaccine strain (strain Deventer, PorcilisPRRS, Merck) that replicates scarcely in PAM.
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39 |
24534144
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Thus, in PAM infected with PRRSV strain 3262 the proportion of TLR3+ cells significantly increased from 24h compared with the controls; in contrast strain 3267 resulted in a lower proportion of TLR3+ PAM.
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40 |
25610736
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Aiming to increase the potency of synthetic long peptide (SLP)-based cancer vaccines, the Toll-like receptor 2 (TLR2) ligand Pam3CSK4 was conjugated in a chemically defined fashion to SLPs harbouring both cytotoxic T lymphocyte (CTL) and T helper epitopes.
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