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Hepatocyte DAX1 Deletion Exacerbates Inflammatory Liver Injury by Inducing the Recruitment of CD4⁺ and CD8⁺ T Cells through NF-κB p65 Signaling Pathway in Mice.

ABSTRACT: Fulminant hepatitis is characterized by rapid and massive immune-mediated liver injury. Dosage-sensitive sex reversal-adrenal hypoplasia congenita critical region on the X chromosome, gene 1 (DAX1; NR0B1) represses the transcription of various genes. Here, we determine whether DAX1 serves as a regulator of inflammatory liver injury induced by concanavalin A (ConA). C57BL/6J (WT), myeloid cell-specific Dax1 knockout (MKO), and hepatocyte-specific Dax1 knockout (LKO) mice received single intravenous administration of ConA. Histopathological changes in liver and plasma alanine aminotransferase and aspartate aminotransferase levels in Dax1 MKO mice were comparable with those in WT mice following ConA administration. Unlike Dax1 MKO mice, Dax1 LKO mice

SUBMITTER: Yun HJ

PROVIDER: S-EPMC9698938 | biostudies-literature | 2022 Nov

REPOSITORIES: biostudies-literature

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Hepatocyte DAX1 Deletion Exacerbates Inflammatory Liver Injury by Inducing the Recruitment of CD4⁺ and CD8⁺ T Cells through NF-κB p65 Signaling Pathway in Mice.

OmicsDI is part of the ELIXIR infrastructure

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Dataset Information

Hepatocyte DAX1 Deletion Exacerbates Inflammatory Liver Injury by Inducing the Recruitment of CD4+ and CD8+ T Cells through NF-κB p65 Signaling Pathway in Mice.

OmicsDI is part of the ELIXIR infrastructure

Tweets

Hepatocyte DAX1 Deletion Exacerbates Inflammatory Liver Injury by Inducing the Recruitment of CD4⁺ and CD8⁺ T Cells through NF-κB p65 Signaling Pathway in Mice.