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. 2018 Jan 11;94(1):35–44. doi: 10.2183/pjab.94.003

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© 2018 The Japan Academy

This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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Figure 2. — CD72 regulates the development of lupus-like disease in mice. (A-C) CD72^c, a weak allele, causes moderate lupus-like disease in the C57BL/6 (B6) background in the presence of the Fas^lpr mutation. Representative PAS staining (A) and immunohistochemistry for IgG and C3 (B) of kidney sections, and scores of the severity of glomerulonephritis are shown. Originally published in The Journal of Immunology (Xu, M. et al., 2013). CD72^c is a modifier gene that regulates Fas^lpr-induced autoimmune disease (J. Immunol. 190: 3189–3196, 2013, Copyright© The American Association of Immunologists, Inc.). (D) Severity of the lupus-like disease in C57BL/6 (B6)-Fas^lpr/lpr (lpr) and MRL-Fas^lpr/lpr (lpr) mice shows an inverse correlation with the functional activity of CD72. The MRL background contains additional SLE-causing gene(s) other than CD72^c, because mice with the MRL background show more severe disease than mice with the C57BL/6 background with the same CD72 allele.