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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
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
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
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
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
34 d diminished ear inflammation in response to dinitrofluorobenzene-induced DTH that correlated with a
41 mAb during sensitization with the hapten 2,4-dinitrofluorobenzene resulted in CHS responses of increa
43 aggerated inflammation, and higher levels of dinitrofluorobenzene-specific IgG2a compared with wild-t
46 Generation of contact hypersensitivity to dinitrofluorobenzene, which involves Th1 and CD8(+) effe
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