ライフサイエンスコーパス: autoimmune thyroiditis

1 ptide binding and presentation to T-cells in autoimmune thyroiditis.

2 were highly correlated with the progress of autoimmune thyroiditis.

3 two cases of hyperthyroidism consistent with autoimmune thyroiditis.

4 ier resolution of granulomatous experimental autoimmune thyroiditis.

5 e identification of susceptibility genes for autoimmune thyroiditis.

6 ical investigation that have been applied to autoimmune thyroiditis.

7 h nodes might prevent missing a diagnosis of autoimmune thyroiditis.

8 orts a disease-limiting role of IFN-gamma in autoimmune thyroiditis.

9 ma in the thyroid dysfunction that occurs in autoimmune thyroiditis.

10 also recognized by the sera of patients with autoimmune thyroiditis.

11 f patients showed autoimmune disorders, i.e. autoimmune thyroiditis (26.3%), dermatitis herpetiformis

12 of coexistence of rheumatoid arthritis (RA), autoimmune thyroiditis (AIT), multiple sclerosis (MS), a

13 analysis of hypothyroidism, hyperthyroidism, autoimmune thyroiditis (AIT), serum concentrations of th

14 e co-occurrence of type 1 diabetes (T1D) and autoimmune thyroiditis (AITD).

15 B1 polymorphism determines susceptibility to autoimmune thyroiditis and implicate Tg as an important

16 tive was to evaluate the association between autoimmune thyroiditis and the Delphian lymph node durin

17 ythematosus, 2 had multiple sclerosis, 2 had autoimmune thyroiditis, and 7 had other conditions.

18 how that the regulatory T cells that prevent autoimmune thyroiditis are generated in vivo only when t

19 ease of the Tg-cleaving activity in IgG from autoimmune thyroiditis (ATh) and systemic lupus erythema

20 Further diagnostic work-up revealed autoimmune thyroiditis, but no signs of inflammatory bow

21 Previous studies have shown that autoimmune thyroiditis can be induced in normal laborato

22 with the publication of a paper showing that autoimmune thyroiditis could be induced in animals.

23 dominant peptide when inducing experimental autoimmune thyroiditis (EAT) in NOD mice expressing huma

24 ence of anti-B7.2 had decreased experimental autoimmune thyroiditis (EAT) severity compared with reci

25 -transgenic model (A(-)E(+)) of experimental autoimmune thyroiditis (EAT) that permits disease induct

26 responses to rat neu and mTg with resultant autoimmune thyroiditis (EAT) were both enhanced.

27 Experimental autoimmune thyroiditis (EAT) with granulomatous histopat

28 logous to HLA-DR) predispose to experimental autoimmune thyroiditis (EAT), a classical mouse model of

29 On the other hand, murine experimental autoimmune thyroiditis (EAT), a model for HT, presents a

30 he development of granulomatous experimental autoimmune thyroiditis (EAT), DBA1 mice with a disrupted

31 can prevent the development of experimental autoimmune thyroiditis (EAT), experimental autoimmune my

32 in development of granulomatous experimental autoimmune thyroiditis (EAT), IL-4 gene-disrupted mice e

33 autoimmune diseases, as well as experimental autoimmune thyroiditis (EAT).

34 prevent, but also to suppress, experimental autoimmune thyroiditis (EAT).

35 ted resolution of granulomatous experimental autoimmune thyroiditis (G-EAT) at least in part through

36 Granulomatous experimental autoimmune thyroiditis (G-EAT) is induced by mouse thyro

37 Granulomatous experimental autoimmune thyroiditis (G-EAT) is induced by mouse thyro

38 Granulomatous experimental autoimmune thyroiditis (G-EAT) is induced by mouse thyro

39 When granulomatous experimental autoimmune thyroiditis (G-EAT) was induced in CBA/J or D

40 es, resolution of granulomatous experimental autoimmune thyroiditis (G-EAT) was promoted when thyroid

41 a murine model of granulomatous experimental autoimmune thyroiditis (G-EAT) was used to determine the

42 of the humoral autoimmune response in human autoimmune thyroiditis (Hashimoto's thyroiditis).

43 e investigated their effects on experimental autoimmune thyroiditis in CBA/J mice.

44 of thyroid follicular cells in experimental autoimmune thyroiditis, in a manner similar to what is o

45 Experimental autoimmune thyroiditis, induced in mice after challenge

46 te the incidence and severity of spontaneous autoimmune thyroiditis [iodide-accelerated spontaneous a

47 rticularly prevalent in older women, in whom autoimmune thyroiditis is common.

48 usceptibility and resistance to experimental autoimmune thyroiditis is encoded by MHC H2A genes.

49 The results suggest that spontaneous autoimmune thyroiditis is inhibited in mice expressing t

50 of chickens, which suffers from spontaneous autoimmune thyroiditis, is an excellent animal model for

51 water develop iodine-accelerated spontaneous autoimmune thyroiditis (ISAT) with chronic inflammation

52 thyroiditis [iodide-accelerated spontaneous autoimmune thyroiditis (ISAT)] in NOD.H2(h4) mice.

53 s the development of lymphocytic spontaneous autoimmune thyroiditis (L-SAT) in NOD.H-2h4 mice and inh

54 mates, which develop lymphocytic spontaneous autoimmune thyroiditis (L-SAT), all TGF-beta transgenic

55 lin, to which tolerance is typically lost in autoimmune thyroiditis leading to hypothyroidism.

56 One serious adverse event-autoimmune thyroiditis of grade 2 severity-was reported

57 ) had a prior diagnosis of hypothyroidism or autoimmune thyroiditis, of whom 56 were receiving thyrox

58 Nineteen were found with autoimmune thyroiditis or hypothyroidism, and replacemen

59 treatable causes and comorbidities, such as autoimmune thyroiditis or infections.

60 WT lymphocytes could transfer experimental autoimmune thyroiditis or L-SAT to Tg mice, indicating t

61 combinatorial Ig-gene libraries derived from autoimmune thyroiditis patients and specific for the mai

62 -defective C3H/gld mice, lupus patients, and autoimmune thyroiditis patients.

63 studies have been published in the field of autoimmune thyroiditis (represented by Graves' disease a

64 NOD.H-2h4 mice develop spontaneous autoimmune thyroiditis (SAT) and anti-mouse thyroglobuli

65 y 100% of NOD.H-2h4 mice develop spontaneous autoimmune thyroiditis (SAT) and produce anti-mouse thyr

66 are required for development of spontaneous autoimmune thyroiditis (SAT) in NOD.H-2h4 mice where the

67 Spontaneous autoimmune thyroiditis (SAT) is an organ-specific autoim

68 type (WT) NOD.H-2h4 mice develop spontaneous autoimmune thyroiditis (SAT) when given 0.05% NaI in the

69 of B cells in a murine model of spontaneous autoimmune thyroiditis (SAT), B cells were depleted from

70 the thyroid gland during the early stages of autoimmune thyroiditis suggests a possible effector func

71 stations included atopy, granulomatous rash, autoimmune thyroiditis, the presence of antinuclear anti

72 Both peptides induced experimental autoimmune thyroiditis upon direct challenge of CBA/J mi

73 Importantly, treatment of mice with autoimmune thyroiditis using mouse thyroglobulin (mTg)-p