Delayed Control of Herpes Simplex Virus Infection and Impaired CD4(+) T-cell Migration to the Skin in Mouse Models of DOCK8 Deficiency

Overview

Journal Immunol Cell Biol

Publisher Wiley

Specialties Allergy & Immunology
Cell Biology

Date 2015 Mar 18

PMID 25776845

Citations 9

Authors

Inge E A Flesch

Katrina L Randall

Natasha A Hollett

Hsei Di Law

Lisa A Miosge

Yovina Sontani

Christopher C Goodnow

David C Tscharke

Affiliations

Soon will be listed here.

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.

Citing Articles

DOCK2 Deficiency Causes Defects in Antiviral T-Cell Responses and Impaired Control of Herpes Simplex Virus Infection.

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