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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
8 inosa type IV pili and the glycosphingolipid asialo-GM1 (aGM1) can mediate bacterial adherence to epi
9 glycoproteins (e.g. CD8) and the glycolipid asialo-GM1 also carry PNA receptors, although to a much
10 ouse NK cells express the surface glycolipid asialo GM1 and are implicated in the rejection of hetero
11 gangliosides devoid of sialic acids, such as asialo-GM1 and asialo-GM2, and the GM2 derivatives whose
12 Unexpectedly, protection sensitive to anti-asialo-GM1 and increased NK activity were still present
13 e seen in mice treated with anti-NK1.1, anti-asialo GM1, and selected Ly49 subtype-depleted mice.
15 in diameter) in nude mice treated with anti-asialo GM1 antibodies and in severe combined immunodefic
16 immunodeficiency mice by administering anti-asialo GM1 antibodies before subcutaneous tumor injectio
17 ice, broad-spectrum oral antibiotics or anti-asialo GM1 antibodies reduce the expression of IFN-gamma
20 e depletion of NK cells during EAM with anti-asialo GM1 antibody significantly increased myocarditis
22 depleted of NK cells by treatment with anti-asialo GM1 antibody, and such animals did not develop TE
24 onoclonal antibody or with NK-depleting anti-asialo GM1 antisera restored virulence of the mutant vir
27 determined by selective depletion with anti-asialo-GM1 antiserum in vivo and NK-cell-mediated cytoly
30 that it was abrogated by treatment with anti-asialo-GM1 but not anti-CD8, and was induced by CD1(-/-)
34 anied by infiltrations of CD45+, Mac-1+, and asialo-GM1+ cells into the tumor; B220+ cells were prese
38 with rabbit anti-asialo GM anti-serum (alpha-asialo GM1), for in vivo depletion of endogenous NK cell
40 enzymes transfer fucose not only to GM1 and asialo-GM1 (Gg4) but also to galactosyl globoside (Gb5)
41 side series GM1, GM2, GM3, GD1A, GD1B, GT1B, asialo GM1, globotriosyl ceramide, and lactosyl ceramide
42 in gangliosides, gangliosides GM2 or GM3, or asialo-GM1 had weak inhibitory effects on alpha-synuclei
43 emonstrate that SCID mice treated with alpha-asialo GM1 have reduction in the number of asialo GM1-ex
45 6F10 melanoma in SCID mice treated with anti-asialo-GM1 in the absence of a mononuclear infiltration,
46 ould also be depleted by treatment with anti-asialo-GM1, indicating that NK cells were responsible fo
49 (NK) cell function with antibodies to either asialo GM1 or NK 1.1 reversed IL-12 inhibition of basic
51 K-depleted (injected intravenously with anti-asialo GM1) or mock-depleted (injected intravenously wit
52 mice were immunodepleted of T lymphocytes or asialo GM1-positive cells, the restraint on dormant diss
55 sidual host T cells, such that NK1.1+ or DX5+asialo-GM1+ T cells become the predominant T cell subset
56 d that protection afforded by NK1.1+ and DX5+asialo-GM1+ T cells derived from either donors or hosts
59 splenic cell suspensions derived from alpha-asialo GM1-treated SCID mice show lower cytotoxicity aga
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