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. Author manuscript; available in PMC: 2016 May 1.
Published in final edited form as: J Immunol. 2015 Mar 23;194(9):4130–4143. doi: 10.4049/jimmunol.1403023

Figure 1. Suppression of ANA production in B6.Sle1b mice overexpressing B6-derived CD84 and Ly108.

Figure 1

(A) Schematic of the six B6-derived BACs (Bacterial Artificial Chromosomes) spanning the Sle1b interval. Each BAC harbors B6 alleles that genetically complement the indicated region in the Sle1b interval. Founders had variable copy numbers (low copy (1–2), med copy (3–4), and high copy (>10)). (B) Six BACs carrying the B6 alleles of the Sle1b genes were crossed to B6.Sle1b mice and two-three founder lines for each BAC were analyzed for IgG-specific ANA positivity at 7 months of age. Statistical analysis was performed using logistic regression (SAS version 9.1). (C) IgG ANA titers were assessed in 7 month old BAC transgenic mice. Dotted line represents the value that is four standard deviations above the mean titer from B6 mice. ANA titers in Sle1b-BAC25 and Sle1b-BAC90 mice were significantly higher than B6.Sle1b (p<0.01 and p<0.001, respectively). *p <0.05, **p <0.01, ***p <0.001.