ライフサイエンスコーパス: insulin autoantibody

1 inistration and/or also suppresses preformed insulin autoantibodies.

2 lerance, as indicated by failure to generate insulin autoantibodies.

3 IFN-gamma-secreting cells and a decrease in insulin autoantibodies.

4 ages of disease indicated by markers such as insulin autoantibodies.

5 zygous knockout mice spontaneously expressed insulin autoantibodies.

6 of both insulin 1 and 2 to NOD mice induced insulin autoantibodies.

7 ot H-2(b)) results in the rapid induction of insulin autoantibodies.

8 siblings/offspring) and be positive for anti-insulin autoantibodies.

9 hain, and proinsulin peptides did not induce insulin autoantibodies.

10 /c mice, even without adjuvant, could induce insulin autoantibodies.

11 ealed the HLA-associated early appearance of insulin autoantibodies (1-3 years of age) and the later

12 t the TR-->FO checkpoint, 2) abrogated serum insulin autoantibodies, 3) reduced the severity of islet

13 NOD mice spontaneously develop anti-insulin autoantibodies and diabetes.

14 esulting Ptpn22(R619W) mice showed increased insulin autoantibodies and earlier onset and higher pene

15 es with at least 2 autoantibodies, including insulin autoantibodies and normal glucose tolerance, wer

16 betes is often preceded by the appearance of insulin autoantibodies and the reports that prophylactic

17 persistent IA (GAD antibody, IA-2A, or micro insulin autoantibodies) and 84 of them progressed to T1D

18 D mice resistant to insulitis, production of insulin autoantibodies, and onset of type 1 diabetes.

19 Induction of insulin autoantibodies by TRAV5D-4 alpha-chains was abro

20 Fewer transgenic mice were positive for insulin autoantibodies compared with controls.

21 Induced anti-insulin autoantibodies could not be absorbed with the pe

22 so observed as early as 4 wk, prior to mouse insulin autoantibody detection.

23 ciated biochemically defined autoantibodies (insulin autoantibody, GAD antibody, or IA-2 antibody), a

24 k for type 1 diabetes for the development of insulin autoantibodies, glutamic acid decarboxylase 65 (

25 Blood draws for the detection of insulin autoantibody, glutamic acid decarboxylase autoan

26 BCA was defined as elevated levels of insulin autoantibody, glutamic acid decarboxylase autoan

27 otype, before insulitis appears, we measured insulin autoantibodies (IAA) between 3 and 5 wk of age i

28 cell antibody (ICA)-positive relatives with insulin autoantibodies (IAA) or low first-phase insulin

29 t study; these children developed persistent insulin autoantibodies (IAA), GAD autoantibodies (GADA),

30 A subset of children develops persistent insulin autoantibodies (IAA; almost always as the only i

31 With the development of an insulin autoantibody (IAA) assay performed in 96-well fi

32 A total of 85 islet cell antibody (ICA)+ or insulin autoantibody (IAA)+ relatives of patients with t

33 -DRB5 alleles to type 1 diabetes risk and to insulin autoantibody (IAA), GAD65 (GAD autoantibody [GAD

34 (43 laboratories) was 58% (50-74%), and for insulin autoantibody (IAA; 23 laboratories) was 36% (13-

35 ied in the first positive sample as insulin (insulin autoantibody [IAA]) in 180, as GAD (GAD antibody

36 6:A-dKO mice rapidly restored development of insulin autoantibodies (IAAs) and insulitis, despite the

37 Insulin autoantibodies (IAAs) are often present in human

38 ion demonstrated that initial titers of anti-insulin autoantibodies (IAAs) could account for some (P

39 We measured insulin autoantibodies (IAAs), GAD autoantibodies (GAAs)

40 and Ab responses (islet cell autoantibodies, insulin autoantibodies, insulinoma-associated protein-2

41 ith only the altered insulin did not develop insulin autoantibodies, insulitis or autoimmune diabetes

42 Our study shows that higher anti-insulin autoantibody levels at diagnosis can distinguish

43 treatment is also associated with lower anti-insulin autoantibody levels in part by inhibition of T f

44 pment of diabetes in risk subjects with high insulin autoantibody levels.

45 ulin-binding BND2 cells correlated with anti-insulin autoantibody levels.

46 islet cell cytoplasmic autoantibody- and/or insulin autoantibody-negative first-degree relatives of

47 When commenced in already insulin autoantibody(+) NOD mice, continuous BAFFR-Fc tr

48 le reversal of hyperglycemia, and decline in insulin autoantibody positivity was an immune biomarker

49 lood glucose concentrations (<350 mg/dL) and insulin autoantibody positivity were predictors of the s

50 Excluding those with only insulin autoantibody positivity, which is confounded by

51 locks germinal center formation, spontaneous insulin autoantibody production, and type 1 diabetes in

52 with an increase in GC B cells and augmented insulin autoantibody production.

53 he population of CD11b+ cells, and modulated insulin autoantibody production.

54 10 transduction attenuated the production of insulin autoantibodies, quantitatively reduced pancreati

55 s (r = 0.82, P < 0.0001), but minimally with insulin autoantibodies (r = 0.20, P = 0.05) and not with

56 3 Abs were accompanied by low levels of anti-insulin autoantibodies, reduced numbers of islet-associa

57 incomplete Freund's adjuvant enhanced their insulin autoantibody response with a higher level and lo

58 nfiltration, beta-cell destruction, and anti-insulin autoantibodies that mimic early human T1D.

59 IgG insulin autoantibodies that predict type 1 diabetes and

60 No hypoglycemia, IgE responses to insulin, autoantibodies to glutamic acid decarboxylase o

61 Spontaneous anti-insulin autoantibody was blunted in Bcl6fl/fl-CD4.Cre.NO

62 served T cell receptor alpha-chain generates insulin autoantibodies when transgenically or retrogenic

63 Induction of insulin autoantibodies with the B9-23 peptide was observ