ライフサイエンスコーパス: DLE

1 DLE-SLE+ subjects had higher IgG autoantibodies against

2 9), SLE subjects with DLE (DLE+SLE+) (N=10), DLE subjects without SLE (DLE+SLE-) (N=11), and healthy

3 oassays in DLE-SLE+ (N=18), DLE+SLE+ (N=17), DLE+SLE- (N=23), and healthy subjects (N=22).

4 odies using immunoassays in DLE-SLE+ (N=18), DLE+SLE+ (N=17), DLE+SLE- (N=23), and healthy subjects (

5 .2 contains a di-acidic ER exit signal, (280)DLE(282), which promotes concentration of the channel in

6 Although DLE usually responds to topical or intralesional cortico

7 Healthy and DLE+SLE- subjects expressed higher IgM autoantibodies ag

8 ies against selected antigens in healthy and DLE+SLE- subjects may be nonpathogenic.

9 5) allele in combined cutaneous LE (SCLE and DLE) patients with PLE was 42%, significantly lower than

10 al GST gene polymorphisms and PLE, SCLE, and DLE in a case-control study.

11 and desmoglein-3 compared with DLE+SLE+ and DLE-SLE+ subjects.

12 s coated with the Fc-optimized CD33 antibody DLE-HuM195 reveals a distinct kinetic profile.

13 DLE (DLE-SLE+) (N=9), SLE subjects with DLE (DLE+SLE+) (N=10), DLE subjects without SLE (DLE+SLE-) (N

14 tibody profiles of SLE subjects without DLE (DLE-SLE+) (N=9), SLE subjects with DLE (DLE+SLE+) (N=10)

15 Discoid lupus erythematosus (DLE) is a chronic variant of cutaneous lupus erythematos

16 y of choice for discoid lupus erythematosus (DLE) is the 4-aminoquinolone antimalarial hydroxychloroq

17 Discoid lupus erythematosus (DLE) is the most common skin manifestation of lupus.

18 ) patients with discoid lupus erythematosus (DLE) were reported to have milder disease.

19 osus (SCLE) and discoid lupus erythematosus (DLE), which may reflect a common genetic background.

20 eous manifestations, targeted treatments for DLE are lacking, likely because of a dearth of knowledge

21 e support investigations into treatments for DLE that target Th1 cells or the IFN-gamma signaling pat

22 iple mutation Ser293Asp/Ala330Leu/Ile332Glu (DLE), and developed Time-lapse Imaging Microscopy in Nan

23 G autoantibodies against nuclear antigens in DLE+SLE+ versus DLE-SLE+ subjects suggest that DLE indic

24 s without that for IL-17-associated genes in DLE.

25 pressed autoantibodies using immunoassays in DLE-SLE+ (N=18), DLE+SLE+ (N=17), DLE+SLE- (N=23), and h

26 Da) compared with all other groups including DLE+SLE+ subjects (P<0.05).

27 h of knowledge of the molecular landscape of DLE skin.

28 Extraction of T cells from the skin of DLE patients identified a predominance of IFN-gamma-prod

29 Here, we profiled the transcriptome of DLE skin in order to identify signaling pathways and cel

30 nts with treatment-refractory, biopsy-proved DLE were prescribed a novel, off-label preparation of ta

31 (DLE+SLE+) (N=10), DLE subjects without SLE (DLE+SLE-) (N=11), and healthy controls (N=11).

32 ticosteroids and/or oral antimalarials, some DLE is resistant to these treatments or adverse effects

33 E+SLE+ versus DLE-SLE+ subjects suggest that DLE indicates lower disease severity.

34 Further comparison of the DLE transcriptome with that of psoriasis, a useful refer

35 We demonstrate that the DLE-HuM195 antibody increases both the quality and the q

36 antigens progressively rose from healthy to DLE-SLE+ subjects.

37 being used in a lotion formulation to treat DLE lesions, resulting in hair regrowth.

38 against nuclear antigens in DLE+SLE+ versus DLE-SLE+ subjects suggest that DLE indicates lower disea

39 NK cells encountering targets coated with DLE-HuM195 induce rapid target cell apoptosis by promoti

40 k cognate 70, and desmoglein-3 compared with DLE+SLE+ and DLE-SLE+ subjects.

41 tential therapeutic option for patients with DLE that is refractory to first-line therapies and who r

42 d pharmacogenetic study of 200 patients with DLE treated with hydroxychloroquine.

43 hout DLE (DLE-SLE+) (N=9), SLE subjects with DLE (DLE+SLE+) (N=10), DLE subjects without SLE (DLE+SLE

44 utoantibody profiles of SLE subjects without DLE (DLE-SLE+) (N=9), SLE subjects with DLE (DLE+SLE+) (