ライフサイエンスコーパス: ACPA

1 ACPA and anti-CarP antibodies were measured on stored se

2 ACPA status is associated with specific environmental fa

3 ACPA targeting could provide novel insight into importan

4 ACPA were produced by cultured B cells from RA patients,

5 ACPA-positive patients with RA had a significantly highe

6 ACPAs are produced in the absence of identified T cell r

7 ACPAs targeting citrullinated vimentin and histone were

8 ions were also seen in a subanalysis of 1092 ACPA-negative patients (HAQ 0.15, 0.02-0.29; DAS28 0.37,

9 on 77 (p = 2.7 x 10(-8), OR = 0.85) in 7,279 ACPA(+) RA case and 15,870 control subjects.

10 Immunochip data in a discovery set of 2,406 ACPA(-) RA case and 13,930 control individuals.

11 these findings in an independent set of 427 ACPA(-) case subjects, carefully phenotyped with a highl

12 in first-degree relatives positive for >/=9 ACPAs (OR 5.00, 95% CI 1.37-18.18).

13 donor controls, in which positivity for >/=9 ACPAs had 92% specificity and 62% sensitivity for RA.

14 As (number positive, and positivity for >/=9 ACPAs) and RA-related characteristics were examined.

15 irst-degree relatives were positive for >/=9 ACPAs.

16 by measuring anti-citrullinated protein Ab (ACPA) titers in patients' sera.

17 ntibodies against citrullinated protein Ags (ACPA) are associated with the development of rheumatoid

18 h amino acid sites drove risk of ACPA(+) and ACPA(-) disease, the effects of individual residues at H

19 ribute to mounting evidence that ACPA(+) and ACPA(-) RA are genetically distinct and potentially have

20 ociation of ABL with RA disease activity and ACPA concentrations, including multiple antigen-specific

21 ROS-CII reactivity between ACPA-positive and ACPA-negative patients with RA, with 93.8% and 91.6% of

22 alis was associated with ESR (P = 0.046) and ACPAs (P = 0.04).

23 iation between IgG against P. gingivalis and ACPAs in pre-RA and markers of RA activity in individual

24 Anti-citrullinated peptide antibodies (ACPA) have been suggested for early diagnosis.

25 Anti-citrullinated protein antibodies (ACPA) predict increased disease activity and disability

26 ll as anti-citrullinated protein antibodies (ACPA)-positive and negative RA patients.

27 actor, anticitrullinated protein antibodies (ACPAs), and RA activity were measured.

28 ls of anti-citrullinated protein antibodies (ACPAs), antinuclear antibodies (ANAs), anti-tissue trans

29 ce of anti-citrullinated protein antibodies (ACPAs).

30 dies (anti-citrullinated protein antibodies [ACPA]), we demonstrate that the odds ratios and aggregat

31 ed with anti-citrullinated protein antibody (ACPA) levels.

32 ed with anti-citrullinated protein antibody (ACPA) titers.

33 ncluded anti-citrullinated protein antibody (ACPA)-positive patients with arthralgia (n = 58 serum sa

34 tis, in anti-citrullinated protein antibody (ACPA)-positive rheumatoid arthritis (RA) patients versus

35 ncluded anti-citrullinated protein antibody (ACPA; by second-generation anti-cyclic citrullinated pep

36 T cells specific for citrullinated antigens: ACPAs could arise because PADs are recognized by T cells

37 aps even in susceptible individuals that are ACPA-seropositive in human arthritis.

38 c anti-citrullinated protein autoantibodies (ACPA) coexist in the joints of rheumatoid arthritis (RA)

39 on anti-citrullinated protein autoantibody (ACPA)-positive RA risk (p = 1.4 x 10(-9)), which demonst

40 ifference in anti-ROS-CII reactivity between ACPA-positive and ACPA-negative patients with RA, with 9

41 ivity was assessed, and associations between ACPAs (number positive, and positivity for >/=9 ACPAs) a

42 nt pathogenic potential of IC including both ACPA and IgM or IgA RF was established.

43 lification of TNF-alpha secretion induced by ACPA-IC, showing its major implication in the effects of

44 When stimulated by ACPA-IC formed in the presence of IgM RF or IgA RF fract

45 within atherosclerotic plaques, and certain ACPAs are associated with the atherosclerotic burden.

46 -dependent effects of ACPA immune complexes (ACPA-IC).

47 aneous FcR triggering by these RF-containing ACPA-IC and TLR4 ligation possibly makes a major contrib

48 pha response of macrophages to RF-containing ACPA-IC.

49 Cutoffs for positivity for each ACPA were determined using receiver operating characteri

50 arthritis (RA), identifying HLA alleles for ACPA-negative (ACPA(-)) RA has been challenging because

51 get citrullinated autoantigens described for ACPA, we generated a multiepitope citrullinated peptide

52 ategorized as high risk (n = 38) if they had ACPA or positive findings >/=2 assays for RF.

53 Greater ABL was associated with higher ACPA, consistent with findings at articular sites.

54 formation to ACPA and in particular identify ACPA-negative patients with poor prognosis.

55 In ACPA-positive and rheumatoid arthritis subgroups, anti-C

56 of a GRS based on 28 non-HLA risk alleles in ACPA+ cases partially overlaps with ACPA- subgroup of RA

57 s, whereas such antibodies were not found in ACPA(-) patients.

58 s toward amino acid replacement mutations in ACPA(+) antibodies and by their loss of reactivity to ci

59 he IgD(-)CD27(-) memory B-cell population in ACPA(+) RA.

60 trullinated autoantigens in the investigated ACPA(+) RA patients, whereas such antibodies were not fo

61 ti-CCP-2) demonstrate reactivity to multiple ACPAs, and the presence of an increasing number of ACPAs

62 , identifying HLA alleles for ACPA-negative (ACPA(-)) RA has been challenging because of clinical het

63 e of IgM or IgA RF increased the capacity of ACPA-IC to activate the complement cascade.

64 the FcR- and complement-dependent effects of ACPA immune complexes (ACPA-IC).

65 onstitute the basis for a new mouse model of ACPA-positive RA.

66 ine the role of B cells in the production of ACPA in patients with RA.

67 Although both amino acid sites drove risk of ACPA(+) and ACPA(-) disease, the effects of individual r

68 This suggests a model for the emergence of ACPAs in the absence of detectable T cells specific for

69 and the presence of an increasing number of ACPAs may be associated with signs of joint inflammation

70 ck-years of smoking, an increasing number of ACPAs was directly associated with the presence of >/=1

71 us geminatus correlated with the presence of ACPAs/rheumatoid factor.

72 The prevalence of ACPAs and ANAs was higher in RA cases compared to contro

73 verse ancestry divided into subsets based on ACPA status and emphasizes the utility of linking EHR cl

74 identify studies that reported 2 x 2 data on ACPA for the diagnosis of rheumatoid arthritis (by 1987

75 citrullinated-protein-autoantibody-positive (ACPA(+)) rheumatoid arthritis (RA), identifying HLA alle

76 s tested also had B cells that could produce ACPA.

77 Antibodies targeting citrullinated proteins (ACPAs [anticitrullinated protein antibodies]) are common

78 Autoantibodies to citrullinated proteins (ACPAs) are present in two-thirds of patients with rheuma

79 In first-degree relatives, ACPA reactivity was assessed, and associations between A

80 carefully phenotyped with a highly sensitive ACPA assay, and 1,691 control subjects (HLA-DRbeta1 Ser1

81 -based assay was used to measure 16 separate ACPAs in sera from 111 antibody-positive first-degree re

82 Serum ACPA was measured using second-generation anticyclic cit

83 s significantly associated with higher serum ACPA concentration (P = 0.004), 28-joint Disease Activit

84 Antigen-specific ACPA responses were compared among ABL tertiles using si

85 rations, including multiple antigen-specific ACPA.

86 platform to assess distinct antigen-specific ACPA.

87 e GEE adjusted for age, sex, smoking status, ACPA, and year of recruitment to NOAR: beta coefficient

88 odels of RA; however, the exact role of such ACPA ICs in RA pathogenesis has remained elusive.

89 results contribute to mounting evidence that ACPA(+) and ACPA(-) RA are genetically distinct and pote

90 RF-mediated recruitment of more IgG into the ACPA-IC.

91 provide additional prognostic information to ACPA and in particular identify ACPA-negative patients w

92 ell immunization to PAD proteins may trigger ACPAs through a hapten/carrier mechanism.

93 dy to investigate a novel mechanism by which ACPAs specifically targeting citrullinated fibrinogen ma

94 We also identified an association with ACPA(+) RA at HLA-A position 77 (p = 2.7 x 10(-8), OR =

95 leles in ACPA+ cases partially overlaps with ACPA- subgroup of RA cases.

96 icantly higher than that among patients with ACPA-positive arthralgia, patients with OA, and healthy

97 Nearly two-thirds of patients with ACPA-positive RA have immune complexes that contain citr

98 antibodies or pooled IgG from patients with ACPA-positive RA.

99 P. gingivalis was associated with ACPAs (P = 0.04).

100 gingivalis-specific IgG2 was associated with ACPAs (P = 0.049) and disease severity visual analog sca

101 and adjust for clinical heterogeneity within ACPA(-) RA and observed independent associations for ser