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1                                              DNCB induced CHS in humans, whereas at similar doses DNT
2                                              DNCB-specific T-cell clones were raised from 2 subjects,
3 -myrisate 13-acetate, lipopolysaccharide and DNCB-treated human keratinocytes induce interferon-gamma
4 ersensitivity, and the activation of CD91 by DNCB-modified HSP90 proteins could mediate this process.
5                                 By contrast, DNCB required GST facilitation to react with gluthathion
6 ion of DNCB, leaving residual non-detoxified DNCB free to bind to proteins.
7 ntact allergen, 1-chloro-2,4-dinitrobenzene (DNCB), elicits contact hypersensitivity through binding
8 ctase inhibitor 1-chloro-2,4-dinitrobenzene (DNCB), in embryonic rat heart (H9c2) cells, evoked 8 or
9 similar chemicals, 2,4-dinitrochlorobenzene (DNCB) and 2,4-dinitrothiocyanobenzene (DNTB), differ in
10                    2,4-Dinitrochlorobenzene (DNCB) is widely used in human clinical studies and in ex
11 ry syndrome) using 2,4-dinitrochlorobenzene (DNCB) skin testing as part of the initial evaluation.
12 onse to the hapten 2,4-dinitrochlorobenzene (DNCB) which can sensitize all immunocompetent people.
13 ous application of 2,4-dinitrochlorobenzene (DNCB), a small, highly lipophilic chemical sensitizer.
14 ypersensitivity to 2,4-dinitrochlorobenzene (DNCB), in ten PLE patients and 11 controls.
15 irway inflammation and dinitrochlorobenzene (DNCB)-induced CHS models.
16 nsitization model with dinitrochlorobenzene (DNCB) to gain insight into the unique immune phenotype o
17                           However, following DNCB sensitization, DNTB elicited CHS in vivo and stimul
18 DNCB-HSP90 binding plays a role in mediating DNCB-induced contact hypersensitivity, and the activatio
19                              After 3 months, DNCB-specific Th2 responses were persistent in individua
20 d glutathione is consumed in detoxication of DNCB, leaving residual non-detoxified DNCB free to bind
21    Subjects were given a sensitizing dose of DNCB, and 3 wk later were exposed to 0.75 and 2 minimum
22                   Moreover, the frequency of DNCB sensitization and allergic contact dermatitis to to
23 cal cysteines in TRPA1 resulted in a loss of DNCB agonism.
24 that the dissimilar sensitizing potencies of DNCB and DNTB in humans are determined by a previously u
25 te cell line THP-1 suppressed the potency of DNCB by >80%.
26 es and BALB/c mice attenuated the potency of DNCB, consistent with the result of HSP90-knockout mice.
27                Next, we successfully reduced DNCB-induced contact hypersensitivity in HSP90-knockout
28 ipopolysaccharides or the contact sensitizer DNCB results in the secretion of immunoprecipitable inte
29                                   Similarly, DNCB activated nonselective TRPA1 current in patch clamp
30 and associated with significantly Th2-skewed DNCB-specific T-cell responses.
31 on, DNTB elicited CHS in vivo and stimulated DNCB-responsive T cells in vitro, suggesting that differ
32  Although both controls and AD made systemic DNCB-specific Th1 responses, these were reduced in AD an
33                         At the doses tested, DNCB showed equal penetration into skin of all groups.
34                                We found that DNCB activates human TRPA1 dose dependently in FLIPR exp
35            Here, we test the hypothesis that DNCB acts as a TRPA1 agonist and thereby evokes allergic
36                Finally, we hypothesized that DNCB-modified HSP90 activates the immune cells through H
37 ein dinitrophenylation in skin revealed that DNCB penetrated into the epidermis, whereas DNTB remaine
38               Altogether, our data show that DNCB-HSP90 binding plays a role in mediating DNCB-induce
39                     The results suggest that DNCB forms multiple haptens with intracellular and extra
40 duction of pro-inflammatory cytokines in the DNCB-induced CHS model.
41                               In contrast to DNCB, DNTB failed to induce emigration of epidermal Lang
42                        Clinical reactions to DNCB were significantly reduced in AD.
43  UVR-induced suppression of sensitization to DNCB in PLE.
44 rall rate of sensitization after one and two DNCB challenges was 32% and 67%, respectively, which is
45 we found nine candidate proteins with unique DNCB-modified peptide fragments.
46 th stage, we observed that patients who were DNCB test positive were significantly less likely to exp
47              However, the mechanism by which DNCB evokes such symptoms is presently unknown.
48 rradiated control site, were challenged with DNCB.
49 had a better overall prognosis compared with DNCB-negative patients.
50 Fourteen healthy adults were sensitized with DNCB; 11 demonstrated positive T-cell responses to the c