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DOCK8 regulates signal transduction events to control immunity.

Abstract：

:Genetic mutations in the gene encoding DOCK8 cause an autosomal recessive form of hyper immunoglobulin E syndrome (AR-HIES), referred to as DOCK8 deficiency. DOCK8 deficiency in humans results in the onset of combined immunodeficiency disease (CID), clinically associated with chronic infections with diverse microbial pathogens, and a predisposition to malignancy. It is now becoming clear that DOCK8 regulates the function of diverse immune cell sub-types, particularly lymphocytes, to drive both innate and adaptive immune responses. Early studies demonstrated that DOCK8 is required for lymphocyte survival, migration and immune synapse formation, which translates to poor pathogen control in the absence of DOCK8. However, more recent advances have pointed to a crucial role for DOCK8 in regulating the signal transduction events that control transcriptional activity, cytokine production and functional polarization of immune cells. Here, we summarize recent advances in our understanding of DOCK8 function, paying particular attention to an emerging role as a signaling intermediate to promote immune responses to diverse external stimuli.

journal_name

Cell Mol Immunol

journal_title

Cellular & molecular immunology

authors

Kearney CJ,Randall KL,Oliaro J

doi

10.1038/cmi.2017.9

subject

Has Abstract

pub_date

2017-05-01 00:00:00

pages

406-411

issue

5

eissn

1672-7681

issn

2042-0226

pii

cmi20179

journal_volume

14

pub_type

杂志文章,评审

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