Display Settings:

Format

Send to:

Choose Destination
    Neurobiol Aging. 2010 Oct;31(10):1732-42. Epub 2008 Dec 5.

    Th1 responses to beta-amyloid in young humans convert to regulatory IL-10 responses in Down syndrome and Alzheimer's disease.

    Source

    Department of Pathology, Case Western Reserve University School of Medicine, Cleveland, OH 44106, USA. kai.loewenbrueck@neuro.med.tu-dresden.de

    Abstract

    A beta(1-42)-specific antibodies and T-cell proliferation point to the existence of a memory response to A beta(1-42) in humans. Using ELISPOT, we studied A beta(1-42)-specific T cells in individuals of various ages, and in subjects with Trisomy 21 or Alzheimer's disease. We show for the first time that A beta(1-42)-specific Th1-type T-cell memory is present in young humans, producing high levels of IFN-gamma and IL-2. With increasing age, the production of IFN-gamma and IL-2 decreases but is not discontinued in healthy subjects and is accompanied by a sharp rise in CD4(+) T-cell-derived regulatory IL-10 production. In contrast, individuals with Trisomy 21 and with Alzheimer's disease produce IL-10 only in the absence of any effector cytokine. This signifies a switch from a Th1 effector to an IL-10 mediated regulatory response.

    (c) 2008 Elsevier Inc. All rights reserved.

    PMID:
    19058879
    [PubMed - indexed for MEDLINE]

      Supplemental Content

      Icon for Elsevier Science

      Save items

      loading

      Recent activity

      Your browsing activity is empty.

      Activity recording is turned off.

      Turn recording back on

      See more...
      Write to the Help Desk