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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
5 th an equimolar mixture of DNFB and [(2)H(3)]DNFB.
6                               In accordance, DNFB-induced ear swelling was reduced by approximately 5
7                                        After DNFB treatment, Gr-1(high) neutrophils and F4/80(+) macr
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
11                                     Although DNFB sensitization of gld/perforin-/- mice induced hapte
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
14                        In contrast, applying DNFB to PAF receptor-deficient mice or mice injected wit
15 njection of stromelysin-1 immediately before DNFB sensitization rescued the impaired CHS response to
16                          Application of both DNFB and DNTB induced apoptotic cell death of DC in the
17                Oral tolerance was induced by DNFB gavage in germ-free and mice deficient in several T
18                    Oral tolerance induced by DNFB gavage was impaired in germ-free mice and TLR4-defi
19 inhibition of subsequent CHS to the chemical DNFB in wild-type, but not in PAF-R-deficient mice.
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
23 ponse, induced by 2,4,-dinitrofluorobenzene (DNFB), in P-selectin-deficient mice.
24  BALB/c mice, both 2,4-dinitrofluorobenzene (DNFB) and FITC induce CHS.
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,
32 e strains of mice when dinitrofluorobenzene (DNFB) is applied to an irradiated skin surface.
33 vity (CHS) responses to dintrofluorobenzene (DNFB) are IFN-gamma-producing CD8(+) T cells, whereas CD
34                  Neutrophil depletion during DNFB sensitization of WT mice markedly increased IL-12-p
35 ated CHS responses were not generated during DNFB sensitization of neutrophil-depleted WT mice treate
36          Transient TGFbeta1 induction during DNFB sensitization increased contact hypersensitivity re
37 from mice treated with anti-CD154 mAb during DNFB sensitization were less stimulatory for hapten-prim
38               BTLA(-/-) mice showed enhanced DNFB-induced CHS and proliferation and IFN-gamma product
39                                         FITC/DNFB skin painting and subsequent enzyme-linked immunosp
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
43 tact sensitizer 2,4 dinitro-1-fluorobenzene (DNFB) to normal skin.
44        Applying 2,4-dinitro-1-fluorobenzene (DNFB) to wild-type mice activated LC migration.
45  (CK) inhibitor 2,4-dinitro-1-fluorobenzene (DNFB).
46 ontact sensitizer 2,4-dinitro-fluorobenzene (DNFB) depends on microbiota/TLRs and evaluated the role
47 nse in a model of 2,4-dinitro-fluorobenzene (DNFB)-induced contact hypersensitivity.
48                       By contrast, following DNFB application to UV-irradiated skin (UV+DNFB), IL-12p
49 4/80+CD11c(-) cells in DLN 3 hours following DNFB application.
50 e ability of intestinal dendritic cells from DNFB-fed mice to inhibit ACD on adoptive transfer.
51              Additionally, chronic itch from DNFB-induced allergic contact dermatitis was decreased b
52 nnot be sensitized against the potent hapten DNFB.
53    Topical application of a reactive hapten, DNFB, augmented dSEARCH and triggered lateral migration
54 rease in MBL2 cell apoptosis was detected in DNFB-treated ears compared with vehicle control.
55 tin contributes to generation of immunity in DNFB-induced contact hypersensitivity.
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
58 osomes blocked the tumor-promoting effect of DNFB.
59 rance was detected by applying 185 microg of DNFB epicutaneously to mice treated 2 wk earlier with a
60 are derivatized with an equimolar mixture of DNFB and [(2)H(3)]DNFB.
61 ociative learning protocol to a rat model of DNFB-induced contact hypersensitivity.
62              Lymphocytes from lymph nodes of DNFB-sensitized stromelysin-1-deficient mice did not pro
63 plications of ARN077 attenuated key signs of DNFB-induced dermatitis in a dose-dependent manner.
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
66 as well as immunologic tolerance to a second DNFB immunization through normal skin.
67          In vivo injection of 6A6 suppressed DNFB-induced CHS and IFN-gamma production of CD8(+) T ce
68 subchronic applications of ARN077 suppressed DNFB-induced inflammation when administered either befor
69                                 We show that DNFB triggers DETC activation and IL-1beta production in
70                                          The DNFB-regulated tumor formation was blocked by early, but
71 when administered either before or after the DNFB challenge.
72                                 However, the DNFB response is Th1-predominant, while the FITC respons
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
77 had no defect in their ability to respond to DNFB.
78 h IL-12 before DNTB application responded to DNFB challenge with a pronounced ear swelling response w
79 ization rescued the impaired CHS response to DNFB in stromelysin-1-deficient mice.
80 icient mice showed a reduced CHS response to DNFB, in bone marrow chimera and adoptive transfer exper
81 MyD88 were unable to mount a CHS response to DNFB.
82 D88 signaling pathway in the CHS response to DNFB.
83 with elevated and elongated CHS responses to DNFB challenge.
84                     Similar CHS responses to DNFB were elicited in wild-type and CD154(-/-) animals.
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)
87 R4 conditions induction of oral tolerance to DNFB through licensing tolerogenic gut DCs.
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
90         Eliciting an immune reaction towards DNFB in wild-type mice, followed by adoptive transfer to
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
93                               Challenge with DNFB lead to an additionally rapid downregulation of Krt
94  or scratching behavior after challenge with DNFB, confirming that this enzyme plays an important rol
95 even when the animals were rechallenged with DNFB.
96                           Sensitization with DNFB or Ox induced lymph node cell populations of CD8+ T
97 ocytes produce IL-1beta when stimulated with DNFB.
98 e recipient mice adoptively transferred with DNFB immunity generated in P-selectin-deficient mice.
99 ificantly lower than in animals treated with DNFB or IL-12 plus DNTB.
100 ated animals compared with mice treated with DNFB or IL-12 plus DNTB.
101 tory T cells isolated from mice treated with DNFB, DNTB, or IL-12 followed by DNTB.
102                         After treatment with DNFB, PCr withdrawal had no effect on the Ca2+ transient

 
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