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

ABSTRACT: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE44815 | GEO | 2013/09/01

SECONDARY ACCESSION(S): PRJNA191950

REPOSITORIES: GEO

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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 [DOCK8_CPM_NKT]

2013-09-01 | GSE44814 | GEO

DOCK8 is critical for the survival and function of NKT cells

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

| PRJNA191947 | ENA

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. Refer to individual Series

2013-09-01 | E-GEOD-44816 | biostudies-arrayexpress

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

2014-06-25 | GSE58765 | GEO

B cells require DOCK8 to elicit and integrate T cell help when antigen is limiting

Project description:Dedicator of cytokinesis 8 (DOCK8) immunodeficiency syndrome is characterized by a failure of the germinal center response, a process involving the proliferation and positive selection of antigen-specific B cells. While DOCK8-deficient B cells are recruited into germinal centers, we find that they are arrested at a light-zone stage. They are unable to respond to T cell–dependent survival and selection signals, and consequently differentiate into plasma cells or memory B cells. Although DOCK8-deficient B cells can acquire and present antigen to initiate activation of cognate T cells, integrin upregulation, B–T cell conjugate formation, and costimulation are insufficient for sustained activation of B and T cells when antigen availability is limited. Our findings provide an explanation for the failure of B cell-dependent humoral responses in DOCK8 immunodeficiency syndrome, and offer insights into how the level of available antigen modulates B–T cell interactions necessary for humoral immune responses and immune memory.

2024-06-11 | GSE269130 | GEO

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