ライフサイエンスコーパス: anti-GBM antibody

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

2 ficient mice by the intravenous injection of 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 s characterized by circulating and deposited anti-GBM antibodies, accompanied by focal necrotizing gl

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

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

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

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

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

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

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

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

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

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