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1 ficient mice by the intravenous injection of anti-GBM antibody.
2 anti-MPO always became detectable before the anti-GBM antibody.
3 ted with anti- glomerular basement membrane (anti-GBM) antibody (Ab) to induce glomerulonephritis (GN
4 s characterized by circulating and deposited anti-GBM antibodies, accompanied by focal necrotizing gl
5 arked reduction in circulating and deposited anti-GBM antibodies, albuminuria, deposits of fibrin in
6 easures, including the levels of circulating anti-GBM antibodies, albuminuria, the deposition of IgG
7 produced no overall reduction in circulating anti-GBM antibodies, although there was a reduction in I
8 dase was given to 15 adults with circulating anti-GBM antibodies and an eGFR <15 ml/min per 1.73m(2).
9 pCol(28-40)-immunized rats produced in vitro anti-GBM antibodies and antinuclear antibodies.
10  of type IV collagen [alpha3(IV)NC1] develop anti-GBM antibodies and focal necrotizing glomerulonephr
11 ino acids results in all rats' demonstrating anti-GBM antibody and severe EAG.
12  of this peptide influences the formation of anti-GBM antibody; and that the presence of asparagine a
13 s specific for glomerular basement membrane [anti-GBM antibodies]), and spontaneous lupus nephritis.
14        Serologic evidence of both p-ANCA and anti-GBM antibodies are becoming more frequently recogni
15          This was supported by the fact that anti-GBM antibodies became detectable only after day 20.
16 lar capillaries, abruptly arrested following anti-GBM antibody deposition via neutrophil FcgammaRIIA
17 s characterized by circulating and deposited anti-GBM antibodies, focal necrotizing glomerulonephriti
18  human, and recombinant sources, we detected anti-GBM antibodies in all Alport patients in varying ti
19  suggest collectively, as a hypothesis, that anti-GBM antibodies in mice only facilitate disease in M
20 ed mouse strains differ in susceptibility to anti-GBM antibody-induced and spontaneous lupus nephriti
21 s are protective disease-associated genes in anti-GBM antibody-induced nephritis and lupus.
22          Indeed, increased susceptibility to anti-GBM antibody-induced nephritis and spontaneous lupu
23  the kidneys of 3 mouse strains sensitive to anti-GBM antibody-induced nephritis were compared with t
24 ase, while agonists dampened the severity of anti-GBM antibody-induced nephritis.
25 mice with anti-glomerular basement membrane (anti-GBM) antibody-induced experimental nephritis were s
26 e identity of alpha3NC1 epitopes targeted by anti-GBM antibodies is strongly influenced by the molecu
27                At d 7 after the injection of anti-GBM antibody, kidneys from alpha7(-/-) mice display
28  after imlifidase infusion, all patients had anti-GBM antibodies levels below the reference range of
29                                   Detectable anti-GBM antibody levels (>/=1 U/ml but <3 U/ml) in a si
30                                  Circulating anti-GBM antibody levels were not reduced, but there was
31 significant reduction in IgG2a but not IgG1, anti-GBM antibody levels, suggesting downregulation of T
32 ha3alpha4alpha5 NC1 hexamers elicited murine anti-GBM antibodies most closely resembling human ARAS a
33             No patients had detectable serum anti-GBM antibody or monoclonal proteins.
34 n the severity of nephritis but no change in anti-GBM antibody production, and 5 mg resulted in a mar
35  Kyoto rats but also triggered a diversified anti-GBM antibody response through "B cell epitope sprea