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1 DNFB sensitization of CD154(-/-) mice primed IFN-gamma-p
2 DNFB treatment also resulted in rapid depletion of appro
3 DNFB-driven chronic ACD was marked by type 2 inflammatio
4 DNFB-sensitized IL-1R(-/-) mice had low CHS responses to
8 inflammatory cytokines and chemokines after DNFB treatment revealed robust changes in genes that are
9 lated IL-10 mRNA as early as 3-6 hours after DNFB application, immediately preceding a decrease of IL
10 he skin to the experimental contact allergen DNFB results in a displacement of the normally occurring
12 wing exposure to DNFB in wild-type mice, and DNFB-induced ear swelling is reduced by approximately 50
13 pepducin treatment models of oxazolone- and DNFB-induced dermatitis, PZ-235 significantly attenuated
15 njection of stromelysin-1 immediately before DNFB sensitization rescued the impaired CHS response to
20 ontact allergen 1-fluoro-2,4-dinitrobenzene (DNFB) resulted in epidermal accumulation of CD8(+) T(RM)
21 application of 1-fluoro-2,4-dinitrobenzene (DNFB) to carcinogen-treated skin led to the development
22 te to elicit CHS, 2,4-dinitrofluorobenezene (DNFB) sensitization of CXCR2(-/-) mice and neutrophil-de
25 amino groups with 2, 4-dinitrofluorobenzene (DNFB) coupled with electrospray ionization mass spectrom
26 sensitized mice to 2,4-dinitrofluorobenzene (DNFB) elicited inflammation, edema, chemokine synthesis
27 l for CHS in which 2,4-dinitrofluorobenzene (DNFB) is used as allergen, we found that gammadelta T ce
28 f BALB/c mice with 2,4-dinitrofluorobenzene (DNFB) or oxazolone (Ox) resulted in increased and prolon
29 atinase B (MMP-9) in a dinitrofluorobenzene (DNFB)-induced model of contact hypersensitivity (CHS).
30 t its related compound dinitrofluorobenzene (DNFB), because DNTB-pretreated mice cannot be sensitized
31 ensitivity response to dinitrofluorobenzene (DNFB) upon primary sensitization at the UV-exposed site,
33 vity (CHS) responses to dintrofluorobenzene (DNFB) are IFN-gamma-producing CD8(+) T cells, whereas CD
35 ated CHS responses were not generated during DNFB sensitization of neutrophil-depleted WT mice treate
37 from mice treated with anti-CD154 mAb during DNFB sensitization were less stimulatory for hapten-prim
40 naling during 2, 4 dinitro-1-fluorobenezene (DNFB) sensitization to induce hapten-specific CD8 effect
41 in response to 2,4-dinitro-1-fluorobenzene (DNFB) required Fas ligand (FasL) and perforin expression
42 tact sensitizer 2,4-dinitro-1-fluorobenzene (DNFB) resulted in a 13-fold increase in CCL27 protein ac
46 ontact sensitizer 2,4-dinitro-fluorobenzene (DNFB) depends on microbiota/TLRs and evaluated the role
53 Topical application of a reactive hapten, DNFB, augmented dSEARCH and triggered lateral migration
56 cytokine-secreting cells remained reduced in DNFB-sensitized mice, even when the animals were rechall
57 n inflammation by one topical application of DNFB following MBL2 inoculation in C57BL/6 mice resulted
59 rance was detected by applying 185 microg of DNFB epicutaneously to mice treated 2 wk earlier with a
64 uated the impact of topically applied THC on DNFB-mediated allergic contact dermatitis in wild-type a
65 estinal migratory CD103(+) DCs carrying oral DNFB, especially the CD103(+)CD11b(+) DC subset expressi
68 subchronic applications of ARN077 suppressed DNFB-induced inflammation when administered either befor
73 ne methiodide, inhibited chronic itch in the DNFB model and the CTCL model, indicating a contribution
74 IL-17, these T cells did not infiltrate the DNFB challenge site to elicit CHS but did infiltrate the
75 e trafficking of the effector T cells to the DNFB challenge site to elicit the response were investig
76 TCs appear in the skin following exposure to DNFB in wild-type mice, and DNFB-induced ear swelling is
78 h IL-12 before DNTB application responded to DNFB challenge with a pronounced ear swelling response w
80 icient mice showed a reduced CHS response to DNFB, in bone marrow chimera and adoptive transfer exper
85 g response without previous sensitization to DNFB, showing that IL-12 can convert the tolerogen DNTB
86 ermate wild-type (WT) mice were subjected to DNFB-induced CHS, severe combined immunodeficient (SCID)
88 ion induced long-lasting unresponsiveness to DNFB, with 88% and 76% inhibition of primary (first chal
89 a markedly impaired CHS response to topical DNFB, although they responded normally to cutaneously ap
91 alone did not upregulate IL-10 mRNA, but UV+DNFB upregulated IL-10 mRNA as early as 3-6 hours after
92 g DNFB application to UV-irradiated skin (UV+DNFB), IL-12p40 mRNA was not upregulated, and DLN IL-12p
94 or scratching behavior after challenge with DNFB, confirming that this enzyme plays an important rol
98 e recipient mice adoptively transferred with DNFB immunity generated in P-selectin-deficient mice.