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1 AITD and PA were associated bidirectionally (P <= 8 x 10
2 AITD was causally associated with impaired erythropoiesi
3 AITD was causally associated with increased erythrocyte
4 AITDs and rheumatologic disorders have significant commo
5 n some people might actually protect against AITD in others, depending on which additional risk varia
13 between specific rheumatologic disorders and AITDs and manifestations of AITDs that mimic rheumatolog
14 usion, the bidirectional association between AITD and PA suggests a shared heritability for these two
16 ave (1) a genetic susceptibility to clinical AITD, along with (2) a separate predisposition to develo
18 ased the risk of autoimmune thyroid disease (AITD) in the RA patients, whereas the FCRL3 risk variant
20 ften detected in autoimmune thyroid disease (AITD), but the mechanisms underlying lymphocyte entry an
22 pondylitis (AS), autoimmune thyroid disease (AITD), multiple sclerosis (MS) and breast cancer (BC).
36 to express HLA-DR molecules harboring either AITD susceptibility or resistance DR pocket sequences.
38 tic variant in CTLA4 that increases risk for AITD in some people might actually protect against AITD
40 ee homozygous carriers of rs781745126-T have AITD, of whom one also has two other T-cell mediated dis
43 pecific epitopes recognized by antibodies in AITD and has confirmed the increased affinity of stimula
44 g, and whose expression has been detected in AITD, is involved in the migration of lymphocytes to the
45 e thyroid, suggest that CCL21 is involved in AITD pathogenesis, and establish TGCCL21 transgenic mice
46 els support a role for the gut microbiota in AITD, which has been confirmed in some reports from huma
47 s the previously identified 6p and 14q loci (AITD-1 and GD-1, respectively), but the Xq (GD-3) and 13
50 data set of 53 multiplex, multigenerational AITD families (323 individuals), using highly polymorphi
53 develop the autoantibodies characteristic of AITD, and they also have (3) a predisposition to develop
54 ther investigate the genetic determinants of AITD, we conducted an association study using a custom-m
57 interactions underlying the pathogenesis of AITD is essential to uncover new therapeutic targets.
59 ls with interferon alpha, a known trigger of AITD, increased TG promoter activity only when it intera
63 trongly and specifically to both recombinant AITD-susceptible HLA-DR3 protein and HLA-DR3 molecules e
64 et 4 was critical for the development of T1D+AITD; all disease-associated amino acids were linked to
65 ignature confers joint susceptibility to T1D+AITD in the same individual by causing significant struc
66 e identified had a marked preference for the AITD-susceptibility DR signatures and not to those signa
70 ntifying genetic variants that predispose to AITD and thyroid cancer, but the increasing prevalence o
71 The susceptibility genes that predispose to AITD can be subdivided into those that affect the immune
76 ong statistical support for a model in which AITD is the result of "hits" along three distinct geneti
81 nded data set of 102 multiplex families with AITD (540 individuals), through use of 400 microsatellit
84 whole-genome linkage study of patients with AITD, in order to identify their susceptibility genes.