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INDUCTION OF IL - 12 IN MICROGLIA BY AMYLOID beta - PEPTIDE IMPLICATIONS FOR ALZHEIMER VACCINATIONS


, : INDUCTION OF IL - 12 IN MICROGLIA BY AMYLOID beta - PEPTIDE IMPLICATIONS FOR ALZHEIMER VACCINATIONS. Society for Neuroscience Abstract Viewer & Itinerary Planner : Abstract No 192 2

The potential therapeutic immunization of Alzheimer patients against the amyloid beta-peptide that accumulates in their brains has garnered attention since feasibility studies in transgenic mice. But human trials were complicated by the development of inflammation in the brains of some subjects. Whereas effectiveness at preventing Abeta deposition correlates with antibody titer in mice, the development of inflammation in humans reportedly did not. This suggests that the response of some individuals to Abeta is tilted towards a cell-mediated vs. humoral response. Interleukin (IL)-12 participates in the switching of T-cell responses and is connected to the development of organ-specific autoimmunity. As an initial step in elucidating IL-12 regulation in relevant models, we tested the influence of aggregated Abeta(1-42) on IL-12 levels in microglia. Primary rat microglia treated with Abeta showed a substantial elevation of IL-12 p40 mRNA by RT-PCR. Protein levels of the p40 subunit were assayed by ELISA in cultures of the N9 mouse microglial cell line, and inductions were compared to nitrite accumulation. Abeta alone was incapable of elevating nitrite levels in these cells and was effective only in combination with interferon-gamma. By contrast, IL-12 p40 levels were elevated approximately 14-fold by Abeta alone and were further augmented by the inclusion of interferon-gamma. These data suggest that one of the factors responsible for T-cell switching is actually induced by Abeta itself and that manipulation of cytokines may have a useful role in promoting beneficial Abeta immunizations.

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