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1 h SLE and AITD (Graves' disease or Hashimoto thyroiditis).
2 in human autoimmune thyroiditis (Hashimoto's thyroiditis).
3 tiation between Graves' disease and painless thyroiditis.
4 ation of susceptibility genes for autoimmune thyroiditis.
5 ded our understanding of the pathogenesis of thyroiditis.
6 igation that have been applied to autoimmune thyroiditis.
7 es that resemble those observed in Hashimoto thyroiditis.
8 before developing hypothyroidism, suggesting thyroiditis.
9 y present in the pathogenesis of Hashimoto's thyroiditis.
10 these families: T1D, RA, SLE, and Hashimoto thyroiditis.
11 ng and presentation to T-cells in autoimmune thyroiditis.
12 sites and in the development of spontaneous thyroiditis.
13 s allowed for the development of spontaneous thyroiditis.
14 sue from patients diagnosed with Hashimoto's thyroiditis.
15 such as the autoimmune disease, Hashimoto's thyroiditis.
16 y correlated with the progress of autoimmune thyroiditis.
17 ase-limiting role of IFN-gamma in autoimmune thyroiditis.
18 T cell response to mTg and failed to develop thyroiditis.
19 thyrocytes, but did not develop spontaneous thyroiditis.
20 nt autoimmune diseases including Hashimoto's thyroiditis.
21 autoimmune disorders, particularly Hashimoto thyroiditis.
22 hyroid dysfunction that occurs in autoimmune thyroiditis.
23 ized by the sera of patients with autoimmune thyroiditis.
24 ti-RT6.1 mAb induced autoimmune diabetes and thyroiditis.
25 -versus-host disease, multiple sclerosis and thyroiditis.
26 ce with mouse or human Tg resulted in severe thyroiditis.
27 t none of the patients actually had subacute thyroiditis.
28 B rats develop spontaneous hyperglycemia and thyroiditis.
29 ht prevent missing a diagnosis of autoimmune thyroiditis.
30 lphian lymph node during different stages of thyroiditis.
31 Eight patients had a history of Hashimoto thyroiditis.
32 f hyperthyroidism consistent with autoimmune thyroiditis.
33 uitary gland), features found in Hashimoto's thyroiditis.
34 pithelial cells of patients with Hashimoto's thyroiditis.
35 h other abnormalities of hyperthyroidism and thyroiditis.
36 like structures is a hallmark of Hashimoto's thyroiditis.
37 ion of granulomatous experimental autoimmune thyroiditis.
38 -3) mm(2)/sec, and in patients with painless thyroiditis 1.46+/-0.22x10(-3) mm(2)/sec, respectively.
39 enile rheumatoid arthritis, 1 with Hashimoto thyroiditis, 1 with psoriasis and iritis, 1 with diabete
41 showed autoimmune disorders, i.e. autoimmune thyroiditis (26.3%), dermatitis herpetiformis (4%) and d
42 d CD (29%) developed ADs (mainly Hashimoto's thyroiditis, 29 cases), compared with a smaller proporti
43 enced ongoing autoimmune problems, including thyroiditis (3), hemolysis (1), thrombocytopenia (4), an
44 ic thyroiditis that mimics human Hashimoto's thyroiditis, a disease where iodine, IFN-gamma, and adhe
45 a (PTC) and thyroid epithelia in Hashimoto's thyroiditis activates nuclear factor-kappa B (NF-kappaB)
46 iabetes, rheumatoid arthritis, lupus, Graves thyroiditis, Addison disease and other autoimmune disord
47 nce of rheumatoid arthritis (RA), autoimmune thyroiditis (AIT), multiple sclerosis (MS), and insulin-
48 hypothyroidism, hyperthyroidism, autoimmune thyroiditis (AIT), serum concentrations of thyroid-stimu
50 ic stimulation in the setting of Hashimoto's thyroiditis and aberrant somatic hypermutation may play
51 between the ultrasonography (US) results of thyroiditis and characteristics of the Delphian lymph no
52 iated with chronic lymphocytic (Hashimoto's) thyroiditis and does not seem to be affected by thyroid
53 me to target tissues involved in Hashimoto's thyroiditis and Graves' disease, we performed ex vivo an
55 hism determines susceptibility to autoimmune thyroiditis and implicate Tg as an important autoantigen
56 is an excellent animal model for Hashimoto's thyroiditis and provides a unique opportunity to investi
57 hyroid-infiltrating T cell of a patient with thyroiditis and specific for a cryptic thyroid-peroxidas
58 evaluate the association between autoimmune thyroiditis and the Delphian lymph node during different
60 ort no linkage between serologic Hashimoto's thyroiditis and thyroid cancer, yet they are limited by
63 both autoimmune hypothyroidism (Hashimoto's thyroiditis) and autoimmune thyrotoxicosis (Graves' dise
64 gkin's lymphoma [NHL]); endocrine (diabetes, thyroiditis); and rheumatologic (Sjogren's syndrome).
69 dal lymphocytes isolated from a patient with thyroiditis, and unexpectedly, thyroid follicular cells
71 e regulatory T cells that prevent autoimmune thyroiditis are generated in vivo only when the relevant
74 thyroxine at position 2553 (T4p2553) induces thyroiditis as well as strong specific T and B cell resp
75 Tg-cleaving activity in IgG from autoimmune thyroiditis (ATh) and systemic lupus erythematosus (SLE)
76 , thymus hyperplasia, autoimmune lymphocytic thyroiditis, autoimmune hemolytic anemia, and colitis.
77 matoid arthritis, Graves' disease, Hashimoto thyroiditis, autoimmune thyroid disease, and systemic lu
78 on self-Ag presentation, not only suppressed thyroiditis but also prevented reemergence of the diseas
79 rther diagnostic work-up revealed autoimmune thyroiditis, but no signs of inflammatory bowel disease.
81 Previous studies have shown that autoimmune thyroiditis can be induced in normal laboratory rats aft
84 2: indeterminate cases; Group 3: established thyroiditis cases; Group 4: advanced-late stage thyroidi
85 utonomously functioning thyroid nodules, and thyroiditis caused by inflammation, which results in rel
86 ase (TPO), a region frequently recognized in thyroiditis, cDNA sequences coding for peptide fragments
87 mice treated with Flt3-L showed more severe thyroiditis characterized by enhanced lymphocytic infilt
88 TD), Graves' disease and chronic lymphocytic thyroiditis (CLT) are amongst the most common endocrine
90 umatoid arthritis, Graves disease, Hashimoto thyroiditis, Crohn disease, ulcerative colitis, systemic
92 eptide when inducing experimental autoimmune thyroiditis (EAT) in NOD mice expressing human DRbeta1-A
93 i-B7.2 had decreased experimental autoimmune thyroiditis (EAT) severity compared with recipients of c
94 model (A(-)E(+)) of experimental autoimmune thyroiditis (EAT) that permits disease induction with he
98 e other hand, murine experimental autoimmune thyroiditis (EAT), a model for HT, presents a clear link
99 ent of granulomatous experimental autoimmune thyroiditis (EAT), DBA1 mice with a disrupted IFN-gamma
100 t the development of experimental autoimmune thyroiditis (EAT), experimental autoimmune myasthenia gr
101 ent of granulomatous experimental autoimmune thyroiditis (EAT), IL-4 gene-disrupted mice expressing t
105 ion of granulomatous experimental autoimmune thyroiditis (G-EAT) at least in part through regulation
109 When granulomatous experimental autoimmune thyroiditis (G-EAT) was induced in CBA/J or DBA/1 mice,
110 ion of granulomatous experimental autoimmune thyroiditis (G-EAT) was promoted when thyroid epithelial
111 del of granulomatous experimental autoimmune thyroiditis (G-EAT) was used to determine the role of TG
112 erse events (myositis in addition to grade 3 thyroiditis, grade 3 hepatitis, grade 3 pneumonia, and g
113 Fifty percent of the strains susceptible to thyroiditis had a unique SNP haplotype at exons 10 and 1
116 expression of ICAM-1 in this mouse model of thyroiditis, highlighting the complex interplay present
118 One such gene implicated in Hashimoto's thyroiditis (HT) is HLA-DR3, but the association is weak
119 comprising Graves disease (GD) and Hashimoto thyroiditis (HT), develop as a result of a complex inter
120 cluding Graves' disease (GD) and Hashimoto's thyroiditis (HT), is one of the most common of the immun
122 include Graves disease (GD) and Hashimoto's thyroiditis (HT); although these diseases contrast clini
127 xistence of CD4(+)CD25(+) T cells regulating thyroiditis in E(+)B10.Ab(0) (A(-)E(+)) and B10 (A(+)E(-
130 differentiate Graves' disease from painless thyroiditis in patients with untreated thyrotoxicosis.
131 ajor role in the expression of insulitis and thyroiditis in the BB rat, that Th1 lymphocytes may pred
132 ore the challenge to determine their role in thyroiditis in the presence of both H2A and H2E genes.
134 r, whether treatment can prevent post-partum thyroiditis in women who are or have been antibody posit
135 follicular cells in experimental autoimmune thyroiditis, in a manner similar to what is observed in
136 disorders, Graves disease (GD) and Hashimoto thyroiditis, in which perturbations of immune regulation
138 depletion of CD4(+)CD25(+) T cells enhanced thyroiditis induction in the context of either H2E or H2
139 ditionally resistant B10 (H2(b)) mice permit thyroiditis induction with mouse thyroglobulin (mTg) aft
141 sed risk for autoimmune disorders, including thyroiditis, inflammatory bowel disease, rheumatoid arth
143 dermatomyositis, Graves' disease, Hashimoto thyroiditis, insulin-dependent diabetes mellitus, inflam
144 dence and severity of spontaneous autoimmune thyroiditis [iodide-accelerated spontaneous autoimmune t
145 r important causes of thyrotoxicosis include thyroiditis, iodine-induced and drug-induced thyroid dys
149 The lymphocytic infiltration of Hashimoto's thyroiditis is frequently associated with papillary thyr
150 The lymphocytic infiltration of Hashimoto's thyroiditis is frequently encountered in thyroid glands
152 results suggest that spontaneous autoimmune thyroiditis is inhibited in mice expressing transgenic T
154 s, which suffers from spontaneous autoimmune thyroiditis, is an excellent animal model for Hashimoto'
155 op iodine-accelerated spontaneous autoimmune thyroiditis (ISAT) with chronic inflammation of the thyr
157 opment of lymphocytic spontaneous autoimmune thyroiditis (L-SAT) in NOD.H-2h4 mice and inhibits the d
158 h develop lymphocytic spontaneous autoimmune thyroiditis (L-SAT), all TGF-beta transgenic (Tg) mice g
161 pressive effect of H2A genes on H2E-mediated thyroiditis mirrors previous reports of H2E suppression
162 mmune neutropenia, n = 1) and other tissues (thyroiditis, n = 3; psoriasis, n = 2; Graves disease, n
163 ld block the continuous T-cell activation in thyroiditis needed to maintain the autoimmune response t
167 or diagnosis of hypothyroidism or autoimmune thyroiditis, of whom 56 were receiving thyroxine therapy
169 n-autoimmune IIT can manifest as destructive thyroiditis or as hypothyroidism with negative thyroid a
170 (MS), autoimmune thyroid disease (Hashimoto thyroiditis or Graves disease), juvenile RA, inflammator
173 ce, which developed an extensive lymphocytic thyroiditis or insulitis that nevertheless did not elimi
174 cytes could transfer experimental autoimmune thyroiditis or L-SAT to Tg mice, indicating that the tra
175 ied associations with additional phenotypes: thyroiditis (OR = 0.58, p = 1.4 x 10(-5)), nodular (OR =
177 al Ig-gene libraries derived from autoimmune thyroiditis patients and specific for the main autoantig
180 odine increases the incidence of Hashimoto's thyroiditis, perhaps by augmenting the antigenicity of t
181 autoimmune diseases, including scleroderma, thyroiditis, primary biliary cirrhosis, Sjogren syndrome
183 ng thyroidectomy with coexisting Hashimoto's thyroiditis report an increased prevalence of papillary
184 ve been published in the field of autoimmune thyroiditis (represented by Graves' disease and Hashimot
185 We previously reported that in wild-type, thyroiditis-resistant BALB/c mice that underwent regress
187 OD.H-2h4 mice develop spontaneous autoimmune thyroiditis (SAT) and anti-mouse thyroglobulin (MTg) aut
188 OD.H-2h4 mice develop spontaneous autoimmune thyroiditis (SAT) and produce anti-mouse thyroglobulin a
189 ed for development of spontaneous autoimmune thyroiditis (SAT) in NOD.H-2h4 mice where they function
191 OD.H-2h4 mice develop spontaneous autoimmune thyroiditis (SAT) when given 0.05% NaI in their drinking
192 in a murine model of spontaneous autoimmune thyroiditis (SAT), B cells were depleted from adult NOD.
194 significant difference in the prevalence of thyroiditis, Sjogren's syndrome, or Hodgkin's or NHL.
195 yroid lymphomas in patients with Hashimoto's thyroiditis strongly suggests a pathogenetic link betwee
196 row transplantation, patient 1 had Hashimoto thyroiditis, suggesting that organ-specific autoimmunity
197 icularly either Graves' disease or Hashimoto thyroiditis, suggesting the possibility of different pat
198 gland during the early stages of autoimmune thyroiditis suggests a possible effector function of CD1
199 spontaneously develop autoimmune lymphocytic thyroiditis that mimics human Hashimoto's thyroiditis, a
200 ifferentiating Graves' disease from painless thyroiditis, the best result was obtained with area unde
201 ogenetic process of autoimmune (Hashimoto's) thyroiditis, the most common cause of hypothyroidism in
202 cluded atopy, granulomatous rash, autoimmune thyroiditis, the presence of antinuclear antibodies, sin
203 ed where the initial impression was subacute thyroiditis, there was a clinical response to prednisone
207 oth peptides induced experimental autoimmune thyroiditis upon direct challenge of CBA/J mice with pep
208 portantly, treatment of mice with autoimmune thyroiditis using mouse thyroglobulin (mTg)-pulsed anti-
209 minority of CS patients, include Hashimoto's thyroiditis, vascular malformations and mental retardati
212 rom macroglobulinemia, cryoglobulinemia, and thyroiditis were all <.0038, the Bonferroni threshold fo
214 and mice spontaneously developed destructive thyroiditis with histological, clinical and hormonal sig
215 12 induced severe, destructive granulomatous thyroiditis with neutrophil inflammation, fibrin deposit
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