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2017 ; 14
(5
): 406-411
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DOCK8 regulates signal transduction events to control immunity
#MMPMID28366940
Kearney CJ
; Randall KL
; Oliaro J
Cell Mol Immunol
2017[May]; 14
(5
): 406-411
PMID28366940
show ga
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.