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 autoantibodies from patients with autoimmune anti-GBM disease.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

33 2 to provide sustained expression, effective anti-GBM cytotoxicity, and minimal neurotoxicity.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

48 46 can induce T cell responses and injury in anti-GBM GN.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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