ライフサイエンスコーパス: DNCB

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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 By contrast, DNCB required GST facilitation to react with gluthathion

5 ion of DNCB, leaving residual non-detoxified DNCB free to bind to proteins.

6 ctase inhibitor 1-chloro-2,4-dinitrobenzene (DNCB), in embryonic rat heart (H9c2) cells, evoked 8 or

7 similar chemicals, 2,4-dinitrochlorobenzene (DNCB) and 2,4-dinitrothiocyanobenzene (DNTB), differ in

8 2,4-Dinitrochlorobenzene (DNCB) is widely used in human clinical studies and in ex

9 ry syndrome) using 2,4-dinitrochlorobenzene (DNCB) skin testing as part of the initial evaluation.

10 onse to the hapten 2,4-dinitrochlorobenzene (DNCB) which can sensitize all immunocompetent people.

11 ous application of 2,4-dinitrochlorobenzene (DNCB), a small, highly lipophilic chemical sensitizer.

12 ypersensitivity to 2,4-dinitrochlorobenzene (DNCB), in ten PLE patients and 11 controls.

13 irway inflammation and dinitrochlorobenzene (DNCB)-induced CHS models.

14 nsitization model with dinitrochlorobenzene (DNCB) to gain insight into the unique immune phenotype o

15 However, following DNCB sensitization, DNTB elicited CHS in vivo and stimul

16 After 3 months, DNCB-specific Th2 responses were persistent in individua

17 d glutathione is consumed in detoxication of DNCB, leaving residual non-detoxified DNCB free to bind

18 Subjects were given a sensitizing dose of DNCB, and 3 wk later were exposed to 0.75 and 2 minimum

19 Moreover, the frequency of DNCB sensitization and allergic contact dermatitis to to

20 cal cysteines in TRPA1 resulted in a loss of DNCB agonism.

21 that the dissimilar sensitizing potencies of DNCB and DNTB in humans are determined by a previously u

22 ipopolysaccharides or the contact sensitizer DNCB results in the secretion of immunoprecipitable inte

23 Similarly, DNCB activated nonselective TRPA1 current in patch clamp

24 and associated with significantly Th2-skewed DNCB-specific T-cell responses.

25 on, DNTB elicited CHS in vivo and stimulated DNCB-responsive T cells in vitro, suggesting that differ

26 Although both controls and AD made systemic DNCB-specific Th1 responses, these were reduced in AD an

27 At the doses tested, DNCB showed equal penetration into skin of all groups.

28 We found that DNCB activates human TRPA1 dose dependently in FLIPR exp

29 Here, we test the hypothesis that DNCB acts as a TRPA1 agonist and thereby evokes allergic

30 ein dinitrophenylation in skin revealed that DNCB penetrated into the epidermis, whereas DNTB remaine

31 The results suggest that DNCB forms multiple haptens with intracellular and extra

32 duction of pro-inflammatory cytokines in the DNCB-induced CHS model.

33 In contrast to DNCB, DNTB failed to induce emigration of epidermal Lang

34 Clinical reactions to DNCB were significantly reduced in AD.

35 UVR-induced suppression of sensitization to DNCB in PLE.

36 rall rate of sensitization after one and two DNCB challenges was 32% and 67%, respectively, which is

37 th stage, we observed that patients who were DNCB test positive were significantly less likely to exp

38 However, the mechanism by which DNCB evokes such symptoms is presently unknown.

39 rradiated control site, were challenged with DNCB.

40 had a better overall prognosis compared with DNCB-negative patients.

41 Fourteen healthy adults were sensitized with DNCB; 11 demonstrated positive T-cell responses to the c

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