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1 that first encounter an Ag in the periphery (cross-tolerance).
2 oss-priming) or in CD8+ T cell inactivation (cross-tolerance).
3 ffective concentration of Cd was considered (cross-tolerance).
4 tion during lipopolysaccharide tolerance and cross tolerance.
5 ignaling is involved in the induction of TLR cross-tolerance.
6 tion of TRIM30alpha and LTbetaR-mediated TLR cross-tolerance.
7 erexpression, suggesting its crucial role in cross-tolerance.
8  TNF-alpha production, mimicking LPS-induced cross-tolerance.
9  LPS-exposed THP-1 monocytes was studied for cross-tolerance.
10 vitro monocytic cell-based endotoxin-induced cross-tolerance.
11  THP1 cells resulted in a state of flagellin cross-tolerance.
12 y closely correlates with the development of cross-tolerance.
13 hine, which may account for the lack of NSIA cross-tolerance.
14 DCs were required for both cross-priming and cross-tolerance.
15 g that LPS and mycobacterial products induce cross-tolerance.
16 o the in vivo phenomena of cross-priming and cross-tolerance.
17 the vehicle previously, indicating a lack of cross-tolerance.
18 redictors explained significant variation in cross-tolerance.
19 mitochondria, which contributes to endotoxin cross-tolerance.
20 ile a genome-wide analysis failed to predict cross-tolerance, a subset of genes facilitated growth in
21 LPS and IL-1 were found to induce a state of cross-tolerance against each other, while no such recipr
22 environments and pathways that contribute to cross-tolerance among metals.
23                        In addition, there is cross-tolerance and cross-dependence between mu, A1, and
24                                 Furthermore, cross-tolerance and cross-withdrawal between mu, A1, and
25                          The observations of cross-tolerance and cross-withdrawal suggest that all th
26 rized human promonocytic THP-1 cells develop cross-tolerance and no longer respond to LTA-induced IL-
27 hment of an in vitro system for the study of cross-tolerance and show that dendritic cells (DCs) phag
28 ent from LPS with regard to the induction of cross-tolerance, and these actions may be mediated, at l
29 Pam3Cys and Ec LPS did not induce a state of cross-tolerance at the level of TNF-alpha.
30 We tested three predictors for the degree of cross-tolerance, based on similarity in 1) the physioche
31 he accentuating effect of ICB CHA suggesting cross-tolerance between adenosine agonists and cannabino
32 ections in patients with CLL and describes a cross-tolerance between endotoxins and tumors.
33  However, a paucity of information exists on cross-tolerance between hemorrhage and sepsis.
34          We also demonstrated that there was cross-tolerance between SP-A and LPS in THP-1 cells.
35 lease, and HLA-DR expression, and induce TLR cross-tolerance by decreased phosphorylation of MAPK pat
36       We outline how single processes (e.g., cross-tolerance) can buffer the effects of multiple stre
37                                      Broader cross-tolerance characterized lines bearing mutations af
38                         To date, LPS-induced cross-tolerance has not been examined regarding microRNA
39                                              Cross-tolerance, in which plants pre-treated with chitin
40 g-SP tolerance via both direct and indirect (cross-tolerance) mechanisms leading to prevention and ef
41  induce direct and most importantly indirect cross-tolerance of alloantigen-specific T cells.
42 limated Daphnia when Cd was removed, and (3) cross-tolerance of Cd-acclimated Daphnia to zinc and sil
43                             We then measured cross-tolerance of each metal-adapted line to the other
44 ontaneous cytotoxic response attributable to cross-tolerance of several unrelated NK-activating recep
45 te that after high-dose cocaine SA, there is cross-tolerance of the DAT to other uptake blockers, but
46 out when adaptation to one stressor provides cross-tolerance or cross-intolerance to other stressors.
47 ogenous antigens and can maintain tolerance (cross-tolerance) or induce immune responses (cross-primi
48  either the same (tolerance) or a different (cross-tolerance) oxidant gas.
49 f evidence that NOD2 stimulation activates a cross-tolerance response that downregulates and thus pre
50 opolysaccharide tolerance) or Gram-positive (cross tolerance) stimulus.
51 n of induced tolerance also provides induced cross-tolerance that is not restricted to pesticides wit
52 ingly appreciated that heat shock may induce cross-tolerance to a variety of stimuli based on in vitr
53 ience to heatwaves, associated with improved cross-tolerance to additional acute stressors and involv
54 184 lost its analgesic activity and produced cross-tolerance to cannabinoid receptor (CB1) agonists i
55 to the anticonvulsant action of this drug or cross-tolerance to diazepam.
56 de (LPS) and flagellin may induce a state of cross-tolerance to each other.
57 ular O2.- and prevented tolerance to NTG and cross-tolerance to endogenous nitric oxide released by a
58                                 Induction of cross-tolerance to endotoxin by endogenous cytokines has
59 ration of a low dose of TNF-alpha can induce cross-tolerance to endotoxin by induction of endogenous
60                                  LPS-induced cross-tolerance to flagellin is also associated with a b
61 ce to endotoxin over 7 days, which conferred cross-tolerance to intestinal manipulation.
62 n kinase activity and subsequently conferred cross-tolerance to lipopolysaccharide stimulation.
63 d higher tolerance to carbaryl and increased cross-tolerance to malathion and cypermethrin but not to
64 o evidence was observed for a role of IDO or cross-tolerance to mycobacterial Hsp70, mycobacterial Hs
65 mic morphine administration but did not show cross-tolerance to NSIA.
66 thermal tolerance and the observed extensive cross-tolerance to other environmental stressors.
67 so investigated the ability of LPS to induce cross-tolerance to postoperative ileus.
68 aged extracellular mitochondria (MH) induced cross-tolerance to subsequent endotoxin challenge, where
69 ception and the development of tolerance and cross-tolerance to the antinociceptive effects of opioid
70 tioning of the muscularis showed significant cross-tolerance to the functional, molecular, and leukoc
71                                 In addition, cross-tolerance to the inhibitory effect of the mu-opioi
72 cyclase and suggest a potential mechanism of cross-tolerance to the motor incoordinating effects of c
73 n on bone marrow-derived macrophages induced cross-tolerance to TLR4 and TLR9 ligands in vitro.
74 ages derived from these mice LTbetaR-induced cross-tolerance to TLR4 and TLR9 ligands was impaired.
75 ergence in evolved phenotypes with extensive cross-tolerance to various other environmental stressors
76  state of hyporesponsiveness, referred to as cross-tolerance, to both homologous and heterologous lig
77                                              Cross-tolerance was also demonstrated following 3 days o
78                                  TNF-induced cross-tolerance was dependent on the kinase GSK3, which
79                                              Cross-tolerance was not a characteristic of adr1 plants,
80                                              Cross-tolerance was observed by TLR5 ligand flagellin an
81 han saline-infused rats indicates that kappa cross-tolerance was present.
82                 To explore the potential for cross-tolerance, we adapted Saccharomyces cerevisiae to
83 r antagonist naloxone, and two-way analgesic cross-tolerance with morphine.
84 e effective with meditation due to a lack of cross-tolerance with opiate-based medications.