Presented antigen from damaged pancreatic β cells activates autoreactive T cells in virus-mediated autoimmune diabetes
J. Clin. Invest. Marc S. Horwitz, et al. 109:79 doi:10.1172/JCI11198 [Go to this article.]

Figure 2
(a) Histological analysis of pancreata of treated BDC Tg and NOD mice. Representative sections of the pancreas from STZ-treated BDC Tg mice and poly I:C–treated BDC Tg mice reveal islet cell integrity and function. The function of β cells was confirmed by immunohistochemistry using antibody to insulin (INS) (×400), present as brown staining. Mice were sacrificed at 2 weeks after treatment. (b) Immunohistological analysis of the islets from treated BDC Tg mice for activated T cells. Representative immunostained sections of islets from the pancreas of either STZ- or poly I:C–treated BDC Tg mice. Immunohistochemical staining for either CD4 or CD25 was performed and revealed CD4⁺ lymphocytes in both mice, but only STZ-treated mice have activated CD4⁺ cells as demonstrated by CD25 staining. Immunostained cells are brown (×400). The mice were sacrificed at 14 days after treatment. (c) Immunohistological analysis of pancreata from treated BDC Tg and NOD mice for macrophages. Representative immunostained sections of the pancreas from CB4-infected and STZ- and poly I:C–treated BDC Tg and NOD mice reveal differences in the number and activation state of resident macrophages. Antibody to the macrophage activation marker F4/80 was used to identify activated macrophages, which, following CB4 infection and STZ treatment of BDC Tg mice, appear to become activated in the peri-insular inflammation and to mobilize into the islets of Langerhans during insulitis (×400). Brown anti-macrophage staining is present over macrophages. Mice were sacrificed 2 weeks after infection or treatment.