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1 CB1 receptors attenuate CHS responses to 2,4-dinitrofluorobenzene.
2 ype contact hypersensitivity to the chemical dinitrofluorobenzene.
3 model induced by repeated application of 2,4-dinitrofluorobenzene.
4  followed by a subsequent challenge with 2,4-dinitrofluorobenzene.
5 D8(+) T cells mediating CHS responses to 2,4-dinitrofluorobenzene.
6 l of delayed-type hypersensitivity using 2,4-dinitrofluorobenzene.
7 ring sensitization and elicitation of CHS to dinitrofluorobenzene.
8 -B irradiation on C57BL/6 mice sensitized to dinitrofluorobenzene.
9 gm muscle was progressively inhibited by 2,4-dinitrofluorobenzene.
10 CHS) response to the obligate sensitizer 2,4-dinitrofluorobenzene.
11  contact hypersensitivity (CHS) responses to dinitrofluorobenzene, a type 1 cytokine-mediated immune
12 al contact hypersensitivity responses to 2,4-dinitrofluorobenzene and oxazolone.
13 lammatory cytokine genes in the responses to dinitrofluorobenzene and oxazolone.
14 the effect of the inflammasome activator 2,4-dinitrofluorobenzene, and IL-1beta on TSLP mRNA expressi
15 tact dermatitis after topical application of dinitrofluorobenzene, and show enhanced inflammatory les
16 persensitivity in C57Bl/6 mice utilizing 2,4-dinitrofluorobenzene as the hapten.
17 es at daily intervals and then sensitized to dinitrofluorobenzene at the site of irradiation showed a
18 al protein L23 was derivatized with [3H]2, 4-dinitrofluorobenzene both at the N terminus and at inter
19 arkedly suppressed ear swelling responses to dinitrofluorobenzene challenge.
20                                       In the dinitrofluorobenzene contact hypersensitivity model, UV-
21                     In BALB/c mice, both 2,4-dinitrofluorobenzene (DNFB) and FITC induce CHS.
22 pic labeling of alpha-amino groups with 2, 4-dinitrofluorobenzene (DNFB) coupled with electrospray io
23 ance in UVB-susceptible strains of mice when dinitrofluorobenzene (DNFB) is applied to an irradiated
24  well-established model for CHS in which 2,4-dinitrofluorobenzene (DNFB) is used as allergen, we foun
25 before sensitization of BALB/c mice with 2,4-dinitrofluorobenzene (DNFB) or oxazolone (Ox) resulted i
26  to induce a contact sensitivity response to dinitrofluorobenzene (DNFB) upon primary sensitization a
27 duces tolerance against its related compound dinitrofluorobenzene (DNFB), because DNTB-pretreated mic
28 t hypersensitivity response, induced by 2,4,-dinitrofluorobenzene (DNFB), in P-selectin-deficient mic
29 lysin-1 (MMP-3) or gelatinase B (MMP-9) in a dinitrofluorobenzene (DNFB)-induced model of contact hyp
30                    During sensitization with dinitrofluorobenzene for contact hypersensitivity (CHS)
31 ut not contact hypersensitivity responses to dinitrofluorobenzene for up to 6 wk of ultraviolet radia
32  which is induced by potent sensitizers (ie, dinitrofluorobenzene), human ACD is induced by weak-to-m
33 cant sex differences in the magnitude of 2,4-dinitrofluorobenzene-induced CHS.
34 d diminished ear inflammation in response to dinitrofluorobenzene-induced DTH that correlated with a
35                           In the in vivo 2,4-dinitrofluorobenzene model of inflammation, Nbs1(B/B) an
36                     Graded inhibition by 2,4-dinitrofluorobenzene of intracellular CK activity by up
37  6 hours later mice were sensitized with 2,4-dinitrofluorobenzene on the same dorsal area.
38           We also assessed the effect of 2,4-dinitrofluorobenzene on TSLP and the TH2 response in mic
39 rsensitivity (DTH) reactions to the chemical dinitrofluorobenzene only in PAF-R-expressing mice.
40                                    Replacing dinitrofluorobenzene priming with IFN-alpha stimulation,
41 mAb during sensitization with the hapten 2,4-dinitrofluorobenzene resulted in CHS responses of increa
42                     Exposure to TMA, but not dinitrofluorobenzene, resulted in a robust eosinophil sk
43 aggerated inflammation, and higher levels of dinitrofluorobenzene-specific IgG2a compared with wild-t
44                                         When dinitrofluorobenzene was painted on vinblastine-treated
45 is early CXCL1 production in response to 2,4-dinitrofluorobenzene were investigated.
46    Generation of contact hypersensitivity to dinitrofluorobenzene, which involves Th1 and CD8(+) effe

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