JCI - Increased T cell reactivity to amyloid β protein in older humans and patients with Alzheimer disease

Increased T cell reactivity to amyloid β protein in older humans and patients with Alzheimer disease

Alon Monsonego, Victor Zota, Arnon Karni, Jeffery I. Krieger, Amit Bar-Or, Gal Bitan, Andrew E. Budson, Reisa Sperling, Dennis J. Selkoe, Howard L. Weiner

Published in Volume 112, Issue 3

J Clin Invest. 2003; 112(3):415–422 doi:10.1172/JCI18104

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Figure 3

Epitope specificity and cytokine profile of Aβ-reactive T cell lines. Split-well assays were performed as described in Methods. To generate Aβ-reactive T cell lines, positive wells were restimulated in the presence of irradiated PBMCs and Aβ and then maintained with 10 U/ml IL-2. To determine Aβ and epitope specificity, T cell lines were stimulated with Aβ1–42 and two overlapping peptides, Aβ1–28 or Aβ15–42, followed by their stimulation with nested peptides of the Aβ15–42 region. To measure Aβ-induced cytokine production, supernatants were collected 48 hours after stimulation and examined by ELISA. T cell proliferation of three representative lines is shown: (a–c) induced by Aβ1–42 (a and c) Aβ15–42, and (b) Aβ1–28. T cell proliferation was also induced by (d) Aβ16–30 (e) Aβ19–33, and (f) Aβ28–42. Aβ-induced secretion of IFN-γ and IL-13 is shown in g through l.