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1.
Fig. 2

Fig. 2. From: Immune tolerance induction to enzyme-replacement therapy by co-administration of short-term, low-dose methotrexate in a murine Pompe disease model.

The recombinant human acid α-glucosidase (rhGAA)-specific immunoglobulin (IgG) response declines following chronic weekly rhGAA treatment. Acid α-glucosidase (GAA) knock-out mice were injected weekly with 20 mg/kg of rhGAA. rhGAA-specific IgG was evaluated every other week through week 16 and then monthly through 28 weeks by serum enzyme-linked immunosorbent assay. These data represent a pool of three experiments.

A Joseph, et al. Clin Exp Immunol. 2008 April;152(1):138-146.
2.
Fig. 1

Fig. 1. From: Immune tolerance induction to enzyme-replacement therapy by co-administration of short-term, low-dose methotrexate in a murine Pompe disease model.

The recombinant human acid α-glucosidase (rhGAA)-specific immunoglobulin G (IgG) response following weekly administration of 20 mg/kg rhGAA. (a) Acid α-glucosidase (GAA) knock-out (KO) mice were injected weekly in the peritoneum with 20 mg/kg of rhGAA. These numbers represent the means and standard errors of samples pooled from three experiments. (b) GAA KO mice were injected weekly intravenously with 20 mg/kg of rhGAA. These numbers represent the means and standard errors from 112 mice and 16 experiments. rhGAA-specific IgG was evaluated every other week by serum enzyme-linked immunosorbent assay.

A Joseph, et al. Clin Exp Immunol. 2008 April;152(1):138-146.
3.
Fig. 6

Fig. 6. From: Immune tolerance induction to enzyme-replacement therapy by co-administration of short-term, low-dose methotrexate in a murine Pompe disease model.

The percentage of B1 B cells in the peritoneal cavity increases significantly 24 h following primary recombinant human acid α-glucosidase (rhGAA) administration (20 mg/kg). Peritoneal exudate cells were assessed by flow cytometry analysis for the percentage of B1 B cells (IgMhi, CD23, CD11b+, CD43+). (a) Flow cytometry analysis of peritoneal exudate cells from control and rhGAA-treated acid α-glucosidase (GAA) knock-out mice. (b) Pooled flow cytometry analysis data from three experiments. IgM, immunoglobulin M.

A Joseph, et al. Clin Exp Immunol. 2008 April;152(1):138-146.
4.
Fig. 5

Fig. 5. From: Immune tolerance induction to enzyme-replacement therapy by co-administration of short-term, low-dose methotrexate in a murine Pompe disease model.

A short course of low-dose methotrexate (MTX) treatment can induce a long-lived suppression of recombinant human acid α-glucosidase (rhGAA)-specific immunoglobulin (IgG) responses. Acid α-glucosidase (GAA) knock-out mice were injected weekly for 32 weeks with 20 mg/kg of rhGAA. 5 or 0·5 mg/kg of MTX was administered for either the first 3 or 8 weeks of chronic weekly rhGAA treatment. rhGAA-specific IgG was evaluated every other week to week 16 and then monthly to 32 weeks by serum enzyme-linked immunosorbent assay. Data are representative of three independent similar experiments.

A Joseph, et al. Clin Exp Immunol. 2008 April;152(1):138-146.
5.
Fig. 4

Fig. 4. From: Immune tolerance induction to enzyme-replacement therapy by co-administration of short-term, low-dose methotrexate in a murine Pompe disease model.

The dose and frequency of methotrexate (MTX) treatment can be reduced while maintaining similar efficacy by the addition of a weekly 0 h MTX treatment. Acid α-glucosidase (GAA) knock-out mice were treated with 5 or 10 mg/kg MTX given 0, 24 and 48 h following either the initial three or eight of 16 weekly recombinant human GAA (rhGAA) treatments. rhGAA-specific IgG was evaluated every other week by serum serum enzyme-linked immunosorbent assay. The 0 mg/kg MTX group represents titres pooled from 16 experiments.

A Joseph, et al. Clin Exp Immunol. 2008 April;152(1):138-146.
6.
Fig. 3

Fig. 3. From: Immune tolerance induction to enzyme-replacement therapy by co-administration of short-term, low-dose methotrexate in a murine Pompe disease model.

Neither cyclosporin A with azathioprine (CsA/Aza) nor mycophenolate mofetil (MMF) inhibits recombinant human acid α-glucosidase (rhGAA)-specific immunoglobulin (IgG) responses. (a) Acid α-glucosidase (GAA) knock-out (KO) mice were treated with tapering doses of CsA/Aza. On day 18, GAA KO mice were injected weekly with increasing intravenous doses of rhGAA until therapeutic levels (20 mg/kg) were reached at 4 weeks. Weekly 20 mg/kg treatments of rhGAA were then continued for 8 additional weeks. rhGAA-specific IgG was evaluated every other week by serum enzyme-linked immunosorbent assay (ELISA). Data are representative of three independent experiments. (b) GAA KO mice were treated orally with 100 mg/kg MMF 0, 24 and 48 h following each of the first eight of 16 weekly intravenous rhGAA treatments. rhGAA-specific IgG was evaluated by serum ELISA. Data are representative of three independent experiments.

A Joseph, et al. Clin Exp Immunol. 2008 April;152(1):138-146.

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