B acille Calmette–Guérin/ DNA hsp65 prime‐boost is protective against diabetes in non‐obese diabetic mice but not in the streptozotocin model of type 1 diabetes
Author(s) -
Rosa L. C.,
ChiusoMinicucci F.,
ZorzellaPezavento S. F. G.,
França T. G. D.,
Ishikawa L. L. W.,
Colavite P. M.,
Balbino B.,
Tavares L. C. B.,
Silva C. L.,
Marques C.,
Ikoma M. R. V.,
Sartori A.
Publication year - 2013
Publication title -
clinical & experimental immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.329
H-Index - 135
eISSN - 1365-2249
pISSN - 0009-9104
DOI - 10.1111/cei.12140
Subject(s) - streptozotocin , diabetes mellitus , type 1 diabetes , medicine , prime (order theory) , type 2 diabetes , immunology , endocrinology , mathematics , combinatorics
Summary Type I diabetes is a disease caused by autoimmune destruction of the beta cells in the pancreas that leads to a deficiency in insulin production. The aim of this study was to evaluate the prophylactic potential of a prime‐boost strategy involving bacille Calmette–Guérin ( BCG ) and the pVAXhsp65 vaccine ( BCG / DNA hsp65) in diabetes induced by streptozotocin ( STZ ) in C 57 BL /6 mice and also in spontaneous type 1 diabetes in non‐obese diabetic ( NOD ) mice. BCG / DNA hsp65 vaccination in NOD mice determined weight gain, protection against hyperglycaemia, decreased islet inflammation, higher levels of cytokine production by the spleen and a reduced number of regulatory T cells in the spleen compared with non‐immunized NOD mice. In the STZ model, however, there was no significant difference in the clinical parameters. Although this vaccination strategy did not protect mice in the STZ model, it was very effective in NOD mice. This is the first report demonstrating that a prime‐boost strategy could be explored as an immunomodulatory procedure in autoimmune diseases.
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