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The production of IFN-γ and IL-17 was detected in the immunized mice, but not in the control mice when stimulated with IRBP161-180.

However, the production of IFN-γ and IL-17 was detected only in immunized mice, but not in the control mice when stimulated with IRBP161-180.

CD4+ T cells from Fyn−/− DO11.10 αβTCR Tg mice, however, do not display increased proliferation compared to CD4+ T cells from WT DO11.10 αβTCR Tg mice when stimulated, either in vitro or in vivo, with peptide and APCs [20].

In addition, spleen cells from reconstituted mice that were challenged with K562 produced 12-fold more human IFN-γ (as measure by ELISA) than spleen cells from naïve reconstituted mice when stimulated for 48 hours with polyI C and 3-fold more when stimulated with IL-15 (data not shown).

Macrophages from male and female mice when stimulated with paracoccin displayed similar phagocytic capability, while fungicidal activity was two times more efficiently performed by macrophages from female mice, a fact that was associated with 50% higher levels of nitric oxide production.

A similar effect was observed in cells from the 5-LO−/− naïve mice when stimulated with the antigen.

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Knockdown of prf had no effect on gametocyte production, and microgametocytes from treated mice released gametes effectively when stimulated in vitro.

Likewise, Jurkat E6-1 and EL-4 mouse thymoma cells which when stimulated with Ionomycin and phorbol myristate acetate (PMA) respectively secrete IL-2, were treated with Perna and the supernatants were added to the responder cell line CTLL-2 [ 35- 38].

Furthermore, cells from S100A9 deficient mice display reduced TNFα production when stimulated with LPS, a deficiency that could be restored by addition of extracellular S100A8/A9 [ 29].

This study shows that NOD mouse-derived spleen cells proliferate when stimulated with algal-derived hGAD65, and that the stimulatory activity of algal-derived hGAD65 is comparable to insect cell-derived hGAD65 standard.

In both the CCIA arthritic and treated groups, dose-dependent proliferation of splenic T cells was demonstrated to CII but not to control antigen, while T cells from healthy (un-immunized) mice only proliferated marginally above background when stimulated with CII (Figure 3A).

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