ライフサイエンスコーパス: anti-IgD

1 e phosphorylation following stimulation with anti-IgD.

2 E-producing cells stimulated by injection of anti-IgD.

3 deficient mice make normal IL-4 responses to anti-IgD.

4 duce IgE following in vivo immunization with anti-IgD.

5 e make little or no IL-4 or IgE responses to anti-IgD Ab and beta 2-microglobulin-deficient mice make

6 ized that treatment with IL-4 at the time of anti-IgD Ab injection would decrease B cell death and en

7 in-deficient mice to make an IgE response to anti-IgD Ab is caused by their rapid degradation of anti

8 Injection of mice with a foreign anti-IgD Ab stimulates B and T cell activation that resu

9 Instead, IL-4 treatment before or along with anti-IgD Ab suppressed IgE and IgG1 responses, whereas I

10 aive T cells, to produce IL-4; 3) failure of anti-IgD Ab to induce an IL-4-dependent IgE response in

11 s II-deficient mice to make IgE responses to anti-IgD Ab.

12 proliferated normally in response to dextran-anti-IgD Abs (alpha delta-dex) and membrane-bound, but n

13 eptor cross-linking using dextran-conjugated anti-IgD Abs (alpha delta-dex), B cells lacking both p50

14 ient B cells stimulated with IL-4, IL-5, and anti-IgD Abs conjugated to dextran, a model for T-indepe

15 Second, dextran-conjugated anti-IgD Abs strongly induce Ku expression, which is var

16 Because most anti-IgD-activated B cells die before they can be stimul

17 IgM (anti-mu heavy chain, anti-mu), but not anti-IgD (anti-delta heavy chain, anti-delta), Abs leads

18 anti-CD40 mAb or CD40 ligand, and/or dextran anti-IgD antibodies in combination with various cytokine

19 th dextran-conjugated anti-immunoglobulin D (anti-IgD) antibodies (anti-Ig-dex), a model for B-cell a

20 L-4-/- mice was also induced by injection of anti-IgD antibody.

21 ux calcium in response to either anti-IgM or anti-IgD cross-linking and contain a significantly incre

22 sponse to self-Ag, and upon stimulation with anti-IgD demonstrated rapid phosphotyrosine phosphorylat

23 Addition of IL-4, IL-5, and anti-IgD dextran to the cultures enhances IgA switching

24 sIgM+/sIgD+ B cells pretreated with anti-IgD-dextran or anti-IgM-dextran did not show signif

25 B cell activation with LPS plus anti-IgD-dextran plus IL-5 plus IL-4 plus TGF-beta produ

26 y reduced in response to lipopolysaccharide, anti-IgD-dextran, and CD40, but maturation and immunoglo

27 IgG1 responses, whereas IL-4 injected after anti-IgD enhanced IgE responses.

28 Moreover, anti-IgD-IC-loaded FDCs induced strong polyclonal IgM re

29 However, B cells were activated when anti-IgD-ICs, formed with Fc-specific rabbit anti-rat Ig

30 ional CD4+ T cells to make IL-4 responses to anti-IgD in vivo; in fact, the large IL-4 response made

31 Treatment with anti-IgD induced germline epsilon (g epsilon) transcript

32 Early IL-4 treatment failed to inhibit anti-IgD-induced Ab production in Fas-defective lpr mice

33 tion would decrease B cell death and enhance anti-IgD-induced Ab responses.

34 specificity of cytokine and Ab responses in anti-IgD-injected mice and the normal IgE responses made

35 The anti-IgD mAb induced [Ca2+]i responses were also higher

36 jecting mice with aggregated 33D1, 33D1 plus anti-IgD mAb, or 33D1 plus IL-1 induced an IgG1 anti-rat

37 e identified through the use of anti-IgM and anti-IgD mAbs.

38 ever, the poor responsiveness of lpr mice to anti-IgD made this result difficult to interpret.

39 ion with lipopolysaccharide, CD40 ligand, or anti-IgD plus appropriate cytokines.

40 , in vivo immunization with OVA-alum or goat anti-IgD resulted in elevated serum IgE levels in the Tg

41 nase (PI3K), and show that both anti-IgM and anti-IgD stimulation results in an increase in the anti-

42 D Ab is caused by their rapid degradation of anti-IgD; sustained anti-IgD treatment induces them to m

43 ed mice and the normal IgE responses made by anti-IgD-treated CD1-deficient mice are difficult to rec

44 eir rapid degradation of anti-IgD; sustained anti-IgD treatment induces them to make relatively norma

45 Induction of g epsilon after anti-IgD treatment of IL-4-/- mice was unaffected by sim

46 f early IL-4 treatment on the Ab response to anti-IgD was associated with a rapid, short-lived increa