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. 2001 Aug 20;194(4):519–528. doi: 10.1084/jem.194.4.519

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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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Generation of IL-17R KO mice. (A) A gene targeting vector was constructed that replaces exons 4–11 with a PGK-neo cassette. A thymidine kinase cassette (MC-TK) was inserted into the 5′ end of the vector in the opposite orientation of the IL-17R gene. Exons are depicted as filled boxes. The initiation (ATG) and termination (TAG) codons as well as the transmembrane domain (TM) are indicated. The Asp718 restriction sites and probe used for genomic Southern blot analyses are indicated. (B) Genomic DNAs from wild-type (+/+), IL-17R^+/−, and IL-17R KO mice were digested with Asp718 and subject to Southern blot analysis using the depicted probe. The sizes of the mutant and wild-type alleles are indicated. (C) Analysis of IL-17 binding to wild-type and IL-17R–deficient cells. The binding of IL-17:Fc to wild-type (+/+) and IL-17R–deficient (−/−) spleen cells gated on expression of the T cell markers CD4 or CD8 or the B cell marker CD19 as well as thioglycollate elicited peritoneal exudate cells gated on expression of the granulocytic marker Gr-1 was determined by flow cytometry and shown in the shaded histograms. Background binding to an irrelevant Fc protein is shown in the open histograms.

Generation of IL-17R KO mice. (A) A gene targeting vector was constructed that replaces exons 4–11 with a PGK-neo cassette. A thymidine kinase cassette (MC-TK) was inserted into the 5′ end of the vector in the opposite orientation of the IL-17R gene. Exons are depicted as filled boxes. The initiation (ATG) and termination (TAG) codons as well as the transmembrane domain (TM) are indicated. The Asp718 restriction sites and probe used for genomic Southern blot analyses are indicated. (B) Genomic DNAs from wild-type (+/+), IL-17R^+/−, and IL-17R KO mice were digested with Asp718 and subject to Southern blot analysis using the depicted probe. The sizes of the mutant and wild-type alleles are indicated. (C) Analysis of IL-17 binding to wild-type and IL-17R–deficient cells. The binding of IL-17:Fc to wild-type (+/+) and IL-17R–deficient (−/−) spleen cells gated on expression of the T cell markers CD4 or CD8 or the B cell marker CD19 as well as thioglycollate elicited peritoneal exudate cells gated on expression of the granulocytic marker Gr-1 was determined by flow cytometry and shown in the shaded histograms. Background binding to an irrelevant Fc protein is shown in the open histograms.