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. 2001 Sep 3;194(5):677–684. doi: 10.1084/jem.194.5.677

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© 2001 The Rockefeller University Press

This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/4.0/).

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B7-2 blockade in NOD mice prevents diabetes but induces a peripheral neuropathy (a and b). B7-2–deficient mice (reference 14) were backcrossed to NOD mice for nine generations and then intercrossed to generate B7-2 WT (B7-2^+/+) and B7-2 KO (B7-2^−/−) NOD mice. B7-2^+/+ (n = 10) and B7-2^−/− (n = 10) females were checked weekly for blood glucose levels (a) and B7-2^−/− females and males were checked weekly for clinical signs of neuropathy (hind leg weakness and inability to grasp wire bar lid of cages) (b). Inset: neuropathic mouse displaying deterioration of hind limb control and coordination. (c and d) WT NOD females were treated with 50 μg of anti–B7-2 blocking mAb (GL-1) every other day between 2 to 4 wk of age plus at weeks 5, 6, and 7 (n = 6) or with PBS (n = 5). Incidence of diabetes (c) and neuropathy (d) were evaluated at weekly intervals.