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Unknown,Transcriptomics,Genomics,Proteomics

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DOCK8 is critical for the survival and function of NKT cells

ABSTRACT: This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

ORGANISM(S): Mus musculus

SUBMITTER: Richard Cornall

PROVIDER: E-GEOD-44816 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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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 [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.

Project description:Patients with the dedicator of cytokinesis 8 (DOCK8) immunodeficiency syndrome suffer from recurrent viral and bacterial infections, hyper-immunoglobulin E levels, eczema, and greater susceptibility to cancer. Because natural killer T (NKT) cells have been implicated in these diseases, we asked if these cells were affected by DOCK8 deficiency. Using a mouse model, we found that DOCK8 deficiency resulted in impaired NKT cell development, principally affecting the formation and survival of long-lived, differentiated NKT cells. In the thymus, DOCK8-deficient mice lack a terminally differentiated subset of NK1.1(+) NKT cells expressing the integrin CD103, whereas in the liver, DOCK8-deficient NKT cells express reduced levels of the prosurvival factor B-cell lymphoma 2 and the integrin lymphocyte function-associated antigen 1. Although the initial NKT cell response to antigen is intact in the absence of DOCK8, their ongoing proliferative and cytokine responses are impaired. Importantly, a similar defect in NKT cell numbers was detected in DOCK8-deficient humans, highlighting the relevance of the mouse model. In conclusion, our data demonstrate that DOCK8 is required for the development and survival of mature NKT cells, consistent with the idea that DOCK8 mediates survival signals within a specialized niche. Accordingly, impaired NKT cell numbers and function are likely to contribute to the susceptibility of DOCK8-deficient patients to recurrent infections and malignant disease.

| S-EPMC3778549 | biostudies-literature

DOCK8 is critical for the survival and function of NKT cells

Project description:This SuperSeries is composed of the SubSeries listed below.

2013-09-01 | GSE44816 | GEO

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

2013-09-01 | GSE44814 | GEO

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

2013-09-01 | GSE44815 | GEO

Gene expression profiling analysis of murine Villin-Gremlin villi compared to age-matched control mice

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2014-10-24 | E-GEOD-62307 | biostudies-arrayexpress

DOCK8 is critical for the survival and function of NKT cells

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

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Enhanced oxidative phosphorylation in NKT cells is essential for their survival and function.

Project description:Cellular metabolism and signaling pathways are key regulators to determine conventional T cell fate and function, but little is understood about the role of cell metabolism for natural killer T (NKT) cell survival, proliferation, and function. We found that NKT cells operate distinct metabolic programming from CD4 T cells. NKT cells are less efficient in glucose uptake than CD4 T cells with or without activation. Gene-expression data revealed that, in NKT cells, glucose is preferentially metabolized by the pentose phosphate pathway and mitochondria, as opposed to being converted into lactate. In fact, glucose is essential for the effector functions of NKT cells and a high lactate environment is detrimental for NKT cell survival and proliferation. Increased glucose uptake and IFN-γ expression in NKT cells is inversely correlated with bacterial loads in response to bacterial infection, further supporting the significance of glucose metabolism for NKT cell function. We also found that promyelocytic leukemia zinc finger seemed to play a role in regulating NKT cells' glucose metabolism. Overall, our study reveals that NKT cells use distinct arms of glucose metabolism for their survival and function.

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