ライフサイエンスコーパス: AITD

1 AITDs and rheumatologic disorders have significant commo

2 n some people might actually protect against AITD in others, depending on which additional risk varia

3 he FCRL3 risk variant was protective against AITD.

4 Multipoint analysis, designating all AITD sib pairs as affected, showed a peak NPL score of 3

5 e was at least 1 member who had both SLE and AITD (Graves' disease or Hashimoto thyroiditis).

6 bors a susceptibility gene shared by SLE and AITD.

7 Because T1D and AITD are individually strongly associated with different

8 T1D and AITD frequently occur together in the same individual, a

9 confer joint susceptibility to both T1D and AITD in the same individual (APS3v).

10 between specific rheumatologic disorders and AITDs and manifestations of AITDs that mimic rheumatolog

11 interact with one another to cause clinical AITD.

12 ave (1) a genetic susceptibility to clinical AITD, along with (2) a separate predisposition to develo

13 ased the risk of autoimmune thyroid disease (AITD) in the RA patients, whereas the FCRL3 risk variant

14 ften detected in autoimmune thyroid disease (AITD), but the mechanisms underlying lymphocyte entry an

15 Autoimmune thyroid disease (AITD), including Graves' disease (GD) and Hashimoto's th

16 pondylitis (AS), autoimmune thyroid disease (AITD), multiple sclerosis (MS) and breast cancer (BC).

17 abetes (T1D) and autoimmune thyroid disease (AITD).

18 a high risk for autoimmune thyroid disease (AITD).

19 ngly linked with autoimmune thyroid disease (AITD).

20 rs affected with autoimmune thyroid disease (AITD).

21 Autoimmune thyroid diseases (AITD) arise from complex interactions between genetic, e

22 The autoimmune thyroid diseases (AITD), Graves' disease and chronic lymphocytic thyroidit

23 erring risk for autoimmune thyroid diseases (AITD).

24 Autoimmune thyroid diseases (AITDs) are highly prevalent, affecting 1% to 5% of the p

25 The autoimmune thyroid diseases (AITDs) include two related disorders, Graves disease (GD

26 The autoimmune thyroid diseases (AITDs), comprising Graves disease (GD) and Hashimoto thy

27 architecture of Autoimmune Thyroid Disorder (AITD).

28 Autoimmune thyroid disorders (AITDs) are the most common organ-specific autoimmune dis

29 to express HLA-DR molecules harboring either AITD susceptibility or resistance DR pocket sequences.

30 ncluded that Tg is a susceptibility gene for AITD, both in humans in and in mice.

31 tic variant in CTLA4 that increases risk for AITD in some people might actually protect against AITD

32 wo Tg SNPs conferred susceptibility to human AITD.

33 ld potentially have a role in treating human AITD.

34 pecific epitopes recognized by antibodies in AITD and has confirmed the increased affinity of stimula

35 g, and whose expression has been detected in AITD, is involved in the migration of lymphocytes to the

36 e thyroid, suggest that CCL21 is involved in AITD pathogenesis, and establish TGCCL21 transgenic mice

37 s the previously identified 6p and 14q loci (AITD-1 and GD-1, respectively), but the Xq (GD-3) and 13

38 ve established thyroglobulin (TG) as a major AITD susceptibility gene.

39 The major AITDs include Graves disease (GD) and Hashimoto's thyroi

40 data set of 53 multiplex, multigenerational AITD families (323 individuals), using highly polymorphi

41 We found evidence for seven new AITD risk loci (P < 1.12 x 10(-6); a permutation test de

42 on of the previously reported association of AITD with TSHR and FCRL3.

43 develop the autoantibodies characteristic of AITD, and they also have (3) a predisposition to develop

44 ther investigate the genetic determinants of AITD, we conducted an association study using a custom-m

45 t signatures contribute to the initiation of AITD.

46 LA-DR3, which is key to the pathoetiology of AITD.

47 interactions underlying the pathogenesis of AITD is essential to uncover new therapeutic targets.

48 ibility genes for and the pathophysiology of AITD.

49 ls with interferon alpha, a known trigger of AITD, increased TG promoter activity only when it intera

50 as clinical and laboratory manifestations of AITDs are reviewed.

51 ic disorders and AITDs and manifestations of AITDs that mimic rheumatologic disorders.

52 mic means were employed to identify putative AITD-susceptible HLA-DR3 binders.

53 trongly and specifically to both recombinant AITD-susceptible HLA-DR3 protein and HLA-DR3 molecules e

54 et 4 was critical for the development of T1D+AITD; all disease-associated amino acids were linked to

55 ignature confers joint susceptibility to T1D+AITD in the same individual by causing significant struc

56 e identified had a marked preference for the AITD-susceptibility DR signatures and not to those signa

57 The AITDs are multifactorial and develop in genetically susc

58 1 diabetes (T1D) and autoimmune thyroiditis (AITD).

59 Seven loci showed evidence for linkage to AITD.

60 The susceptibility genes that predispose to AITD can be subdivided into those that affect the immune

61 de polymorphism (SNP) variant predisposes to AITD.

62 FNalpha) and genetic (TG) factors to trigger AITD.

63 atures and not to those signatures that were AITD-protective.

64 ong statistical support for a model in which AITD is the result of "hits" along three distinct geneti

65 roups was more significantly associated with AITD (P < 0.001).

66 on 33 SNP were significantly associated with AITD (P < 0.01).

67 an SNP (-1623A-->G) that was associated with AITD in the Caucasian population (p = 0.006).

68 nded data set of 102 multiplex families with AITD (540 individuals), through use of 400 microsatellit

69 by which environmental factors interact with AITD susceptibility genes.

70 x loci that showed evidence for linkage with AITD in a data set of 56 multiplex families.

71 whole-genome linkage study of patients with AITD, in order to identify their susceptibility genes.