Delayed control of herpes simplex virus infection and impaired CD4(+) T-cell migration to the skin in mouse models of DOCK8 deficiency

Immunology and Cell Biology
Inge E A FleschDavid C Tscharke

Abstract

DOCK8 deficiency in humans and mice leads to multiple defects in immune cell numbers and function. Patients with this immunodeficiency have a high morbidity and mortality, and are distinguished by chronic cutaneous viral infections, including those caused by herpes simplex virus (HSV). The underlying mechanism of the specific susceptibility to these chronic cutaneous viral infections is currently unknown, largely because the effect of DOCK8 deficiency has not been studied in suitable models. A better understanding of these mechanisms is required to underpin the development of more specific therapies. Here we show that DOCK8-deficient mice have poor control of primary cutaneous herpes simplex lesions and this is associated with increased virus loads. Furthermore, DOCK8-deficient mice showed a lack of CD4(+) T-cell infiltration into HSV-infected skin.

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Citations

May 22, 2016·Journal of Clinical Immunology·Qian ZhangHelen C Su
Aug 25, 2016·The Journal of Allergy and Clinical Immunology·Stuart G TangyeCindy S Ma
Aug 11, 2017·The Journal of Immunology : Official Journal of the American Association of Immunologists·Conor J KearneyJane Oliaro
Jan 29, 2017·The Journal of Immunology : Official Journal of the American Association of Immunologists·Meiwan CaoJunko Kimura
Feb 8, 2019·European Journal of Immunology·Alicia S WilsonAnne Brüstle
Dec 20, 2018·Immunological Reviews·Helen C SuAlexandra F Freeman
Jun 17, 2020·Journal of Leukocyte Biology·Yuanyuan ChenChaohong Liu
Dec 20, 2018·Immunological Reviews·Erin Janssen, Raif S Geha
Aug 11, 2018·Mammalian Genome : Official Journal of the International Mammalian Genome Society·Qian ZhangJean-Laurent Casanova

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