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