ライフサイエンスコーパス: asialo-GM1

1 d with subcutaneous (s.c.) injection of anti-asialo GM1.

2 4.61 x 10-12 M for GM1 to 1.88 x 10-10 M for asialo GM1.

3 y), and mice depleted of NK cells using anti-asialo-GM1.

4 by treatment in vitro and in vivo with anti-asialo-GM1.

5 ence: GM1 > GM2 > GD1A > GM3 > GT1B > GD1B > asialo-GM1.

6 ely when NK cells were eliminated using anti-asialo GM1 Ab administration, but only marginally impair

7 Depletion of NK cells with anti-asialo GM1 Ab reduced or abrogated the observed antitumo

8 ion of NK cells (via anti-IL-2Rbeta and anti-Asialo-GM1 Abs) or blockade of the NK cell activating re

9 inosa type IV pili and the glycosphingolipid asialo-GM1 (aGM1) can mediate bacterial adherence to epi

10 glycoproteins (e.g. CD8) and the glycolipid asialo-GM1 also carry PNA receptors, although to a much

11 ouse NK cells express the surface glycolipid asialo GM1 and are implicated in the rejection of hetero

12 gangliosides devoid of sialic acids, such as asialo-GM1 and asialo-GM2, and the GM2 derivatives whose

13 Unexpectedly, protection sensitive to anti-asialo-GM1 and increased NK activity were still present

14 e seen in mice treated with anti-NK1.1, anti-asialo GM1, and selected Ly49 subtype-depleted mice.

15 PE64Delta553pil bound specifically to asialo-GM1, and, when injected into rabbits, produced an

16 in diameter) in nude mice treated with anti-asialo GM1 antibodies and in severe combined immunodefic

17 immunodeficiency mice by administering anti-asialo GM1 antibodies before subcutaneous tumor injectio

18 ice, broad-spectrum oral antibiotics or anti-asialo GM1 antibodies reduce the expression of IFN-gamma

19 ntraperitoneal administration of RB6-8C5 and asialo GM1 antibodies.

20 In vivo depletion of NK cells by anti-asialo GM1 antibody abrogated the antimetastatic effects

21 e depletion of NK cells during EAM with anti-asialo GM1 antibody significantly increased myocarditis

22 We used polyclonal anti-asialo GM1 antibody to actively deplete NK cells in vivo

23 depleted of NK cells by treatment with anti-asialo GM1 antibody, and such animals did not develop TE

24 killer cells was achieved through an IV anti-asialo-GM1 antibody injection.

25 onoclonal antibody or with NK-depleting anti-asialo GM1 antisera restored virulence of the mutant vir

26 Treatment with anti-asialo GM1 antiserum (ASGM1), which ablated circulating

27 SCID mice received rabbit anti-asialo GM1 antiserum to abrogate endogenous natural kill

28 determined by selective depletion with anti-asialo-GM1 antiserum in vivo and NK-cell-mediated cytoly

29 Among these, trNK cells had reduced asialo-GM1 (AsGM1) expression relative to cNK cells, a p

30 of specific markers such as NK1.1, DX5, and asialo-GM1 (ASGM1).

31 that it was abrogated by treatment with anti-asialo-GM1 but not anti-CD8, and was induced by CD1(-/-)

32 rtially by anti-NK1.1 and completely by anti-asialo GM1, but not by anti-CD8, Abs.

33 We demonstrate that asialo GM1(+) CD8(+) cells play a critical role in this

34 of IL-18 appears to be primarily mediated by asialo GM1+ cells.

35 anied by infiltrations of CD45+, Mac-1+, and asialo-GM1+ cells into the tumor; B220+ cells were prese

36 mature T cells, but require B, NK, and other asialo-GM1+ cells.

37 Treatment with anti-asialo GM1 eliminated NK activity in the eye and at nono

38 a-asialo GM1 have reduction in the number of asialo GM1-expressing splenocytes.

39 with rabbit anti-asialo GM anti-serum (alpha-asialo GM1), for in vivo depletion of endogenous NK cell

40 The gangliosides GD1a, GM1, and asialo-GM1 (GA1) are natural components of murine macrop

41 enzymes transfer fucose not only to GM1 and asialo-GM1 (Gg4) but also to galactosyl globoside (Gb5)

42 side series GM1, GM2, GM3, GD1A, GD1B, GT1B, asialo GM1, globotriosyl ceramide, and lactosyl ceramide

43 in gangliosides, gangliosides GM2 or GM3, or asialo-GM1 had weak inhibitory effects on alpha-synuclei

44 emonstrate that SCID mice treated with alpha-asialo GM1 have reduction in the number of asialo GM1-ex

45 on the terminal galactose, but not to GM1 or asialo-GM1 in an enzyme-linked immunosorbent assay.

46 6F10 melanoma in SCID mice treated with anti-asialo-GM1 in the absence of a mononuclear infiltration,

47 ould also be depleted by treatment with anti-asialo-GM1, indicating that NK cells were responsible fo

48 Furthermore, we provide evidence that asialo GM1 is a potentially important therapeutic target

49 mice were depleted of NK/NKT cells with anti-asialo GM1 or anti-NK1.1 Ab.

50 (NK) cell function with antibodies to either asialo GM1 or NK 1.1 reversed IL-12 inhibition of basic

51 Immunodepletion with anti-asialo-GM1 or anti-CD4 during C3L5-CK beta 11 vaccinatio

52 K-depleted (injected intravenously with anti-asialo GM1) or mock-depleted (injected intravenously wit

53 mice were immunodepleted of T lymphocytes or asialo GM1-positive cells, the restraint on dormant diss

54 Asialo-GM1 pretreatment of MDCK monolayers likewise augm

55 Mice depleted of NK cells using anti-asialo GM1 showed decreased survival and higher lung bac

56 sidual host T cells, such that NK1.1+ or DX5+asialo-GM1+ T cells become the predominant T cell subset

57 d that protection afforded by NK1.1+ and DX5+asialo-GM1+ T cells derived from either donors or hosts

58 allografts by treating recipients with anti-asialo GM1 to deplete NK cells.

59 arlier and induced lethality sooner in alpha-asialo GM1-treated animals.

60 splenic cell suspensions derived from alpha-asialo GM1-treated SCID mice show lower cytotoxicity aga

61 By contrast, complex GSLs, such as asialo-GM1, were not required for NK cell viability and