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. 2010 Feb 15;207(2):309–318. doi: 10.1084/jem.20090880

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© 2010 Fu et al.

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.jem.org/misc/terms.shtml). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 3.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/3.0/).

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Figure 4. — Cre/PLCγ1^fl/⁻ mice develop inflammatory/autoimmune disease. (A) Cre/PLCγ1^fl/− mice were smaller than littermate control mice. A pair of 6-wk-old littermates is shown. (B) PLCγ1 deficiency reduced weight gain in Cre/PLCγ1^fl/− mice. Each point represents the mean weight of 7 to 14 female mice. *: P < 0.05. (C) Infiltration of inflammatory cells in the skin and ear (H&E, x200) of Cre/PLCγ1^fl/− mice. Bar, 100 µm. (D) Infiltration of CD3⁺ T cells in the skin and ear (x200) of Cre/PLCγ1^fl/− mice. The slides were analyzed by immunohistochemistry and examined by Nikon Eclipse E600. Bar, 100 µm. (E) Levels of α-double-stranded DNA antibodies and antinuclear antibodies in the serum of symptomatic Cre/PLCγ1^fl/− mice compared with the indicated control mice.