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DOCK8 is critical for the survival and function of NKT cells

ABSTRACT: DOCK8 is critical for the survival and function of NKT cells

PROVIDER: PRJNA191947 | ENA |

REPOSITORIES: ENA

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DOCK8 is critical for the survival and function of NKT cells [DOCK8_CPM_NKT]

Project description:Analysis of DOCK8 deficient animals revealed a key role for this protein the survival and maintenance of natural killer T cells. This work lead to the identification of genes regulated by the guanine exchange factor, DOCK8. Total RNA was extracted from 3 biological replicates of thymic, DOCK8 deficient NKT cells and compared using an Illumina microarray to WT NKT cells.

2013-09-01 | E-GEOD-44814 | biostudies-arrayexpress

DOCK8 is critical for the survival and function of NKT cells [NKT_CD103+]

Project description:Analysis of DOCK8 deficient animals revealed a novel marker of NKT cell development, the integrin CD103. The role of CD103 was further investigated by RNA microarray comparing CD103 negative versus positive NKT cells. Total RNA was extracted from 3 biological replicates of thymic, CD103positive NKT cells and compared using an Illumina microarray to CD103negative NKT cells.

2013-09-01 | E-GEOD-44815 | biostudies-arrayexpress

DOCK8 is critical for the survival and function of NKT cells [NKT_CD103+]

2013-09-01 | GSE44815 | GEO

DOCK8 is critical for the survival and function of NKT cells [DOCK8_CPM_NKT]

2013-09-01 | GSE44814 | GEO

DOCK8 regulates protective immunity by controlling the function and survival of RORγt+ ILCs

Project description:Retinoic-acid receptor-related orphan receptor-γt-positive (RORγt+) innate lymphoid cells (ILCs) produce interleukin (IL)-22 and IL-17, which are critical for protective immunity against enteric pathogens. The molecular mechanism underlying the development and survival of RORγt+ ILCs is not thoroughly understood. Here we show that Dedicator of cytokinesis 8 (DOCK8), a scaffolding protein involved in cytoskeletal rearrangement and cell migration, is essential for the protective immunity against Citrobacter rodentium. A comparative RNA sequencing-based analysis reveals an impaired induction of antimicrobial peptides in the colon of DOCK8-deficient mice, which correlates with high susceptibility to infection and a very low number of IL-22-producing RORγt+ ILCs in their GI tract. Furthermore, DOCK8-deficient RORγt+ ILCs are less responsive to IL-7 mediated signaling, more prone to apoptosis and produce less IL-22 due to a defect in IL-23-mediated STAT3 phosphorylation. Our studies reveal an unsuspected role of DOCK8 for the function, generation and survival of RORγt+ ILCs. Control and DOCK8 KO mice were infected with 2X109 CFU of Citrobacter rodentium and day 8 post infection mice were sacrificed and their colons were harvested (n=5) . Total RNA was purified from the infected colons with RNeasy mini kit (Qiagen). RNA sequencing was performed (pooled RNA sample from five mice in each group) at Genomic Core Facility Southwestern Medical Center, University of Texas.

2014-06-25 | E-GEOD-58765 | biostudies-arrayexpress

DOCK8 regulates protective immunity by controlling the function and survival of RORγt+ ILCs

2014-06-25 | GSE58765 | GEO