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. Author manuscript; available in PMC: 2013 Nov 29.
Published in final edited form as: Cell Rep. 2013 Jul 18;4(2):10.1016/j.celrep.2013.06.036. doi: 10.1016/j.celrep.2013.06.036

Figure 2. Nonubiquitinatable NEMO Knockin Mice Develop Inflammatory Skin Lesions and Splenomegaly.

Figure 2

(A) Gross photograph of a representative 8-month-old nonubiquitinatable NEMO heterozygous female compared with a WT mouse. The nonubiquitinatable NEMO heterozygous mice develop ulcerated and plaque-like lesions distributed throughout the body. Histologically, the plaque-like skin lesions show hyper-keratosis, parakeratosis, keratin pearls, and a hyperproliferative epidermis with rete-ridge-like protrusions into the dermis. Nonlesional skin from the nonubiquitinatable heterozygous NEMO knockin mice shows little histological change relative to WT mice.

(B) qRT-PCR analysis of cytokines from the skin of WT littermates or from lesional or nonlesional skin from heterozygote nonubiquitinatable NEMO knockin mice (n = 3). Cytokines are significantly elevated in both the lesional and nonlesional skin from the nonubiquitinatable NEMO heterozygous mice. SEM, *p < 0.05, ***p < 0.001.

(C) Representative gross picture showing the enlarged spleens present in the heterozygous nonubiquitinatable NEMO female mice relative to WT female littermate control mice. Flow-cytometry gating on the different subsets of splenic immune cells reveals that the percentage of Gr1+CD11b+ cells is greatly increased, suggesting an inflammatory phenotype in the heterozygous nonubiquitinatable NEMO mice.