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 have been found in different isotypes and subclass

8 ACPAs targeting citrullinated vimentin and histone were

9 et of ACPAs in 25% of RA patients, and Mac-1 ACPAs were significantly associated with HLA-DRB1 shared

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

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

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

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

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

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

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

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

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

19 d circulating anticitrullinated protein Abs (ACPA), but neither the respective pathogenic roles of SE

20 lated (~90%) anti-citrullinated protein Abs (ACPAs).

21 f RA patients with flares and (iii) activate ACPA B cells, thereby promoting affinity maturation and

22 ) or the synthetic cannabinoid (CB) agonists ACPA, WIN55,212-2, CP55,940 (CB(1/2)-non-selective) and

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

24 These findings indicate that an ACPA positive at-risk state is associated with multiface

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

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

27 Furthermore, both ACPA(+) and ACPA(-) RA patients had significantly higher total serum

28 citrullinated protein antibodies (ACPA)+ and ACPA- RA patients and identify two peripheral helper T c

29 lood or synovial tissues from both ACPA+ and ACPA- RA patients by single-cell RNA sequencing and iden

30 synovial CD4(+) T cell subsets in ACPA+ and ACPA- RA.

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

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

33 er the respective pathogenic roles of SE and ACPA in RA nor the mechanisms underlying their coassocia

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

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

36 ibrinogen as a common target for both RF and ACPAs, and suggest a new mechanism in RF-mediated autoim

37 ce of anti-citrullinated peptide antibodies (ACPA) and associated disparities in patients with rheuma

38 Anti-citrullinated peptide antibodies (ACPA) are highly specific to RA and assayed with the com

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

40 immune anticitrullinated protein antibodies (ACPA) during preclinical stages of disease and accumulat

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

42 from anti-citrullinated protein antibodies (ACPA)+ and ACPA- RA patients and identify two peripheral

43 from anti-citrullinated protein antibodies (ACPA)+ RA blood.

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

45 with anti-citrullinated protein antibodies (ACPAs) and subclinical inflammatory changes in joints ar

46 ) and anti-citrullinated protein antibodies (ACPAs) are the two most prevalent autoantibodies in rheu

47 nce of anticitrullinated protein antibodies (ACPAs) but the absence of clinically apparent synovitis

48 itis, anti-citrullinated protein antibodies (ACPAs) have been a topic of extensive research.

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

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

51 table anti-citrullinated protein antibodies (ACPAs), implicating oral mucosal inflammation in RA path

52 e for anti-citrullinated protein antibodies (ACPAs), rheumatoid factors, or other autoantibodies.

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

54 ted by anticitrullinated protein antibodies (ACPAs).

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

56 ilst RF targets the Fc region of antibodies, ACPAs target a far broader spectrum of citrullinated pep

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

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

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

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

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

62 ntibodies to citrullinated protein antigens (ACPA), are detectable prior to inflammatory arthritis (I

63 ntibodies to citrullinated protein antigens (ACPA), rheumatoid factor, and symptoms, such as inflamma

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

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

66 Anti-citrullinated protein autoantibodies (ACPA) are diagnostic for rheumatoid arthritis (RA).

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

68 h anti-citrullinated protein autoantibodies (ACPAs) are a hallmark serological feature of rheumatoid

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

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

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

72 ripheral blood or synovial tissues from both ACPA+ and ACPA- RA patients by single-cell RNA sequencin

73 Furthermore, both ACPA(+) and ACPA(-) RA patients had significantly higher

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

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

76 cation criteria (clinical RA) is preceded by ACPA seropositivity for an average of 3-5 years, a perio

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

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

79 re present without elevations in circulating ACPA titers.

80 h the SE facilitates protein citrullination, ACPA production, and bone destruction.

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

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

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

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

85 tive individuals and individuals with early, ACPA positive clinical RA (Early RA).

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

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

88 at risk of rheumatoid arthritis positive for ACPA and rheumatoid factor with inflammatory joint pain

89 od that is designated as 'at-risk' of RA for ACPA-positive individuals who do not display signs of ar

90 red to be a general phenomenon, observed for ACPAs, non-ACPAs, as well as total IgG in rheumatoid art

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

92 orm of RA, correlated with particularly high ACPA, and PAD4 autoantibodies.

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

94 eted by extensively somatically hypermutated ACPAs encoded by RA blood plasmablasts.

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

96 In ACPA- SF, T(PH) cells display lower levels of GPR56 and

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

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

99 to synovitis and joint tissue destruction in ACPA+ RA.

100 cell markers were significantly different in ACPA(+) RA compared to healthy controls, including an in

101 creased risk of developing active disease in ACPA+ RA in a large cohort of patients with treatment-na

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

103 CD27(-)) CD11c(+) B cells were increased in ACPA(+) RA, and there was a trend for elevation in a CXC

104 bclinical inflammation as measured by MRI in ACPA positive arthralgia (ARIAA) study is a randomised,

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

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

107 ing of the synovial CD4(+) T cell subsets in ACPA+ and ACPA- RA.

108 ive analysis among three groups that include ACPA positive individuals without IA (At-Risk), ACPA neg

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

110 ults now demonstrate that certain monoclonal ACPAs therapeutically block arthritis and inflammation i

111 rinogen by a panel of eight human monoclonal ACPAs.

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

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

114 general phenomenon, observed for ACPAs, non-ACPAs, as well as total IgG in rheumatoid arthritis pati

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

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

117 etiopathogenesis, based on the generation of ACPA through the activity of a unique P. gingivalis pept

118 ross-activation targets in the initiation of ACPA production.

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

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

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

122 3, CCL18 and MMP3 in myeloid cell subsets of ACPA- RA compared with ACPA+ RA.

123 pressing immune cells in synovial tissues of ACPA- RA.

124 cently been implicated in the development of ACPAs.

125 nce for pathogenic and protective effects of ACPAs in the context of arthritis.

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

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

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

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

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

131 ucosal inflammation with local production of ACPAs and rheumatoid factors, leading to development of

132 To understand the roles of ACPAs, one needs to consider their immunological propert

133 rullinated Mac-1 was found to be a target of ACPAs in 25% of RA patients, and Mac-1 ACPAs were signif

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

135 the importance of precision therapy based on ACPA status.

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

137 e of positive autoantibodies (antinuclear or ACPA) was significantly higher - without any seroconvers

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

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

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

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

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

143 A positive individuals without IA (At-Risk), ACPA negative individuals and individuals with early, AC

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

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

146 logies, we quantified a total of 19 separate ACPAs in RA-affected case subjects from four cohorts (n

147 Serum ACPA was measured using second-generation anticyclic cit

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

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

150 rations, including multiple antigen-specific ACPA.

151 platform to assess distinct antigen-specific ACPA.

152 To define MHC differences for specific ACPA serologies, we quantified a total of 19 separate AC

153 tic characteristics underlying fine-specific ACPAs, suggesting that RA may be further subdivided beyo

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

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

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

157 oposed RF target epitopes in IgG1 Fc and the ACPA target fibrinogen.

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

159 se findings characterize pathogenesis of the ACPA(+) at-risk stage and support the concept that the d

160 ein RF may act as a precursor from which the ACPA response evolves.

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

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

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

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

165 eloid cell subsets of ACPA- RA compared with ACPA+ RA.

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

167 nes in the synovial tissues of patients with ACPA- RA.

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

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

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

171 Adults (aged >=18 years) with ACPA positivity, joint pain (but no swelling), and signs

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

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

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