ライフサイエンスコーパス: anti-GBM

1 epitope or by truncation, failed to abrogate anti-GBM Ab production, and 2) the anti-GBM Ab, eluted f

2 In conclusion, accelerated anti-GBM glomerulonephritis is severely aggravated in eN

3 We achieved anti-GBM therapeutic efficacy with no overt toxicities u

4 Serologic evidence of both p-ANCA and anti-GBM antibodies are becoming more frequently recogni

5 led a disassociation between the disease and anti-GBM Ab.

6 Compared with control sera-injected mice and anti-GBM-injected A/J, AKR/J, C3H/HeJ, DBA/2J, MRL/MpJ,

7 The studies in serum sickness and anti-GBM nephritis led to an understanding of autoimmune

8 series demonstrates that monotypic atypical anti-GBM recurs in the allograft and supports the idea t

9 ) in this first series of recurrent atypical anti-GBM nephritis after kidney transplantation.

10 autoantibodies from patients with autoimmune anti-GBM disease.

11 ion, anti-HB-EGF Ab administered just before anti-GBM Ab blocked the fall in SNGFR and GFR at 90 minu

12 With the goal of exploring ways to boost anti-GBM immunity, we developed a B cell-based vaccine (

13 nti-PDCD1 antibodies synergistically boosted anti-GBM immunity and prolonged survival in mice.

14 The specificity of kidney-bound anti-GBM alloantibodies from a patient who had autosomal

15 M nephritis was induced in 129x1/svJ mice by anti-GBM serum challenge.

16 e identity of alpha3NC1 epitopes targeted by anti-GBM antibodies is strongly influenced by the molecu

17 Circulating anti-GBM antibody levels were not reduced, but there was

18 produced no overall reduction in circulating anti-GBM antibodies, although there was a reduction in I

19 easures, including the levels of circulating anti-GBM antibodies, albuminuria, the deposition of IgG

20 dase was given to 15 adults with circulating anti-GBM antibodies and an eGFR <15 ml/min per 1.73m(2).

21 ts with bovine GBM also induced a crescentic anti-GBM GN with an increase of renal cortical ERK activ

22 abbit IgG, induced an accelerated crescentic anti-GBM GN.

23 and renal injury in experimental, crescentic anti-GBM nephritis.

24 ino acids results in all rats' demonstrating anti-GBM antibody and severe EAG.

25 s characterized by circulating and deposited anti-GBM antibodies, accompanied by focal necrotizing gl

26 arked reduction in circulating and deposited anti-GBM antibodies, albuminuria, deposits of fibrin in

27 s characterized by circulating and deposited anti-GBM antibodies, focal necrotizing glomerulonephriti

28 Detectable anti-GBM antibody levels (>/=1 U/ml but <3 U/ml) in a si

29 Only study patients had detectable anti-GBM levels in multiple samples before diagnosis (50

30 human, and recombinant sources, we detected anti-GBM antibodies in all Alport patients in varying ti

31 humoral response, only a select few develop anti-GBM disease.

32 of type IV collagen [alpha3(IV)NC1] develop anti-GBM antibodies and focal necrotizing glomerulonephr

33 mice and prime the immune system to develop anti-GBM immunological memory.

34 Kyoto rats but also triggered a diversified anti-GBM antibody response through "B cell epitope sprea

35 nflux, which causes glomerular damage during anti-GBM glomerulonephritis.

36 ated in the urine and kidneys of mice during anti-GBM disease, as well as in mice with spontaneously

37 s difference was even more pronounced during anti-GBM-GN, explaining why an exogenous VEGFA supply fa

38 We also show during anti-GBM GN in ChAT transgenic mice, ChAT expression was

39 deletion system can be used as an effective anti-GBM therapy by inhibiting tumor growth and migratio

40 2 to provide sustained expression, effective anti-GBM cytotoxicity, and minimal neurotoxicity.

41 Elevated anti-GBM levels (>/=3 U/ml) were present in four patient

42 severe glomerulonephritis but also elicited anti-GBM Ab in 76% of the immunized rats after prominent

43 itation further demonstrated that the eluted anti-GBM Ab recognized conformational B cell epitope(s)

44 om patients' tumors and, in so doing, exerts anti-GBM activity ex vivo.

45 ytes prevented the induction of experimental anti-GBM nephritis.

46 lar capillaries, abruptly arrested following anti-GBM antibody deposition via neutrophil FcgammaRIIA

47 In contrast, conditioned media from anti-GBM-treated animals at all time points showed signi

48 Kidney tissue from anti-GBM nephritic mice showed higher levels of integrin

49 erular basement membrane glomerulonephritis (anti-GBM-GN), using two leading mouse strains, 129S2/SvP

50 nducing antiglomerular basement membrane GN (anti-GBM GN) in ChAT transgenic mice.

51 ies that cross-react with human Goodpasture [anti-GBM/anti-alpha3(IV) NC1] autoantibodies, only a few

52 after imlifidase infusion, all patients had anti-GBM antibodies levels below the reference range of

53 ritis in mice passively immunized with human anti-GBM Abs.

54 significant reduction in IgG2a but not IgG1, anti-GBM antibody levels, suggesting downregulation of T

55 n the severity of nephritis but no change in anti-GBM antibody production, and 5 mg resulted in a mar

56 chemoattractant produced by renal cortex in anti-GBM disease.

57 mmation and glomerular endothelium damage in anti-GBM GN.

58 s are protective disease-associated genes in anti-GBM antibody-induced nephritis and lupus.

59 46 can induce T cell responses and injury in anti-GBM GN.

60 e in regulating the inflammatory response in anti-GBM GN and that disruption of the endogenous protec

61 High glucose increased anti-GBM binding compared with normal glucose; this effe

62 pecific for alpha345NC1 hexamers and induced anti-GBM Ab GN.

63 We induced anti-GBM disease in DBA/1, C57BL/6, AKR, and NOD mice wi

64 n anti-glomerular basement membrane-induced (anti-GBM-induced) glomerulonephritis when expressed on m

65 conjugated 800CW dye, were administered into anti-GBM nephritic mice.

66 ted with anti- glomerular basement membrane (anti-GBM) antibody (Ab) to induce glomerulonephritis (GN

67 mice with anti-glomerular basement membrane (anti-GBM) antibody-induced experimental nephritis were s

68 tcomes in anti-glomerular basement membrane (anti-GBM) disease are sparse, and validated tools to aid

69 iology of anti-glomerular basement membrane (anti-GBM) disease before clinical presentation is unknow

70 Anti-glomerular basement membrane (anti-GBM) disease is an organ-specific autoimmune disord

71 is due to anti-glomerular basement membrane (anti-GBM) disease is unknown.

72 ransplant anti-glomerular basement membrane (anti-GBM) disease.

73 Atypical antiglomerular basement membrane (anti-GBM) nephritis can be defined as linear GBM stainin

74 s specific for glomerular basement membrane [anti-GBM antibodies]), and spontaneous lupus nephritis.

75 ha3alpha4alpha5 NC1 hexamers elicited murine anti-GBM antibodies most closely resembling human ARAS a

76 anti-glomerular basement membrane nephritis (anti-GBM), and membranous glomerulonephritis (MGN).

77 cells and may provide new inroads for novel anti-GBM therapeutic strategies.

78 superoxide dismutase as novel biomarkers of anti-GBM disease and lupus nephritis, with stronger corr

79 Herein, a rare case of anti-GBM disease was reported with circulating autoantib

80 es against laminin-521 in the development of anti-GBM disease.

81 is critically involved in the development of anti-GBM GN from acute glomerular injury to irreversible

82 sformed cells and informs the development of anti-GBM invasion strategies.

83 High antibody titers at diagnosis of anti-GBM disease were associated with ultimate loss of r

84 ary hemorrhage, another important feature of anti-GBM disease; this was not correlated with the sever

85 l efforts have been invested in the field of anti-GBM drug discovery in the past decade, success has

86 of glomerular MEK in the accelerated form of anti-GBM GN, providing a possible mechanism of long-term

87 of this peptide influences the formation of anti-GBM antibody; and that the presence of asparagine a

88 munopathogenic processes in the two forms of anti-GBM disease.

89 r basement membrane (GBM) is the hallmark of anti-GBM glomerulonephritis (GN).

90 ons are an underevaluated common hallmark of anti-GBM-GN in mice.

91 ound-dependent histopathological hallmark of anti-GBM-GN, combined with hemolytic anemia and thromboc

92 At d 7 after the injection of anti-GBM antibody, kidneys from alpha7(-/-) mice display

93 ficient mice by the intravenous injection of anti-GBM antibody.

94 ratification may assist in the management of anti-GBM disease.

95 lead to different clinical manifestations of anti-GBM disease.

96 Th2 responses associates with the outcome of anti-GBM disease in mice.

97 tion of finding clues to the pathogenesis of anti-GBM glomerulonephritis.

98 our understanding of the pathophysiology of anti-GBM disease.

99 The presence of anti-GBM, anti-proteinase 3 (PR3), and anti-myeloperoxid

100 ing CXCL16 actions limits the progression of anti-GBM glomerulonephritis even when the disease is est

101 plication to intervene in the progression of anti-GBM GN and in other M omicron/M phi-dominant GN.

102 ase, while agonists dampened the severity of anti-GBM antibody-induced nephritis.

103 g ability is required to steer the wheels of anti-GBM drug discovery endeavors.

104 -transplant nephritis mediated by pathogenic anti-GBM alloantibodies to collagen IV chains present in

105 y IgG subclasses that mediate posttransplant anti-GBM nephritis.

106 es were from patients without posttransplant anti-GBM nephritis, and 10 were from patients with this

107 the pathogenesis of ARAS posttransplantation anti-GBM nephritis and Goodpasture disease.

108 ivatives (compounds 4 and 26) showing potent anti-GBM activity and improved drug distribution in comp

109 tified a novel type of human IgG4-restricted anti-GBM autoantibodies associated with mild nonprogress

110 No patients had detectable serum anti-GBM antibody or monoclonal proteins.

111 immunotherapy exhibits superior and specific anti-GBM activities, reduces off-target drug delivery an

112 ependent initiation blockade and synergistic anti-GBM effects with PP242.

113 dent initiation and demonstrates synergistic anti-GBM properties when combined with the mechanistic t

114 This was supported by the fact that anti-GBM antibodies became detectable only after day 20.

115 suggest collectively, as a hypothesis, that anti-GBM antibodies in mice only facilitate disease in M

116 abrogate anti-GBM Ab production, and 2) the anti-GBM Ab, eluted from the diseased kidneys, reacted o

117 anti-MPO always became detectable before the anti-GBM antibody.

118 We compared the anti-GBM activity of NK cells engineered to express inte

119 s suggest that HB-EGF expressed early in the anti-GBM Ab GN model contributes to the observed acute g

120 microbial Ag may be sufficient to induce the anti-GBM disease.

121 pJ, NOD/LtJ, P/J, SJL/J, and SWR/J mice, the anti-GBM-injected BUB/BnJ, DBA/1J, and 129/svJ mice deve

122 nction impairment during days 7 to 14 of the anti-GBM GN.

123 e GBM TME and driving the suppression of the anti-GBM response.

124 Furthermore, we demonstrated that the anti-GBM Ab was not related to the peptidic B cell epito

125 The mechanisms eliciting these anti-GBM autoantibodies were investigated in mouse model

126 Thus, anti-GBM Ab may actually be a consequence of T cell-medi

127 the kidneys of 3 mouse strains sensitive to anti-GBM antibody-induced nephritis were compared with t

128 ed mouse strains differ in susceptibility to anti-GBM antibody-induced and spontaneous lupus nephriti

129 Indeed, increased susceptibility to anti-GBM antibody-induced nephritis and spontaneous lupu

130 NCA-associated vasculitis is transferable to anti-GBM disease and the renal histology is strongly pre

131 ate that the RRS concept is transferrable to anti-GBM disease.

132 l outcomes in ANCA-associated vasculitis, to anti-GBM disease.

133 f dual EZH2-HSP90 inhibitor 7 as a tractable anti-GBM agent.

134 lpha4alpha5NC1 hexamers of human GBM, unlike anti-GBM autoantibodies, which targeted sequestered alph

135 s9-mediated gene knock-in to express various anti-GBM CAR constructs with T-specific CD3zeta or neutr

136 pCol(28-40)-immunized rats produced in vitro anti-GBM antibodies and antinuclear antibodies.

137 (iv) compound 7 elicited substantial in vivo anti-GBM efficacy in experimental mice xenografted with

138 nusual combination of c-ANCA antibodies with anti-GBM disease, and this association raises complex qu

139 l study involving 30 patients diagnosed with anti-GBM disease and 30 healthy controls matched for the

140 ion of lupus nephritis, 1 was diagnosed with anti-GBM nephritis, and 4 were diagnosed with isolated a

141 e largest assembled cohorts of patients with anti-GBM disease (with 174 patients included in the fina