IL-18, but not IL-12, regulates NK cell activity following intranasal herpes simplex virus type 1 infection.

IL-18, but not IL-12, regulates NK cell activity following intranasal herpes simplex virus type 1 infection. Research Abstract Details 

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IL-18, but not IL-12, regulates NK cell activity following intranasal herpes simplex virus type 1 infection. Abstract Text:

Patrick C Reading,Paul G Whitney,Daniel P Barr,Magdalena Wojtasiak,Justine D Mintern,Jason Waithman,Andrew G Brooks,

Infection of the respiratory tract with HSV type 1 (HSV-1) can have severe clinical complications, yet little is known of the immune mechanisms that control the replication and spread of HSV-1 in this site. The present study investigated the protective role of IL-12 and IL-18 in host defense against intranasal HSV-1 infection. Both IL-12 and IL-18 were detected in lung fluids following intranasal infection of C57BL/6 (B6) mice. IL-18-deficient (B6.IL-18(-/-)) mice were more susceptible to HSV-1 infection than wild-type B6 mice as evidenced by exacerbated weight loss and enhanced virus growth in the lung. IL-12-deficient (B6.IL-12(-/-)) mice behaved similarly to B6 controls. Enhanced susceptibility of B6.IL-18(-/-) mice to HSV-1 infection correlated with a profound impairment in the ability of NK cells recovered from the lungs to produce IFN-gamma or to mediate cytotoxic activity ex vivo. The weak cytotoxic capacity of NK cells from the lungs of B6.IL-18(-/-) mice correlated with reduced expression of the cytolytic effector molecule granzyme B. Moreover, depletion of NK cells from B6 or B6.IL-12(-/-) mice led to enhanced viral growth in lungs by day 3 postinfection; however, this treatment had no effect on viral titers in lungs of B6.IL-18(-/-) mice. Together these studies demonstrate that IL-18, but not IL-12, plays a key role in the rapid activation of NK cells and therefore in control of early HSV-1 replication in the lung.

IL-18, but not IL-12, regulates NK cell activity following intranasal herpes simplex virus type 1 infection. Publishing Authors By Initials

PC Reading,PG Whitney,DP Barr,M Wojtasiak,JD Mintern,J Waithman,AG Brooks,

For similar virus diseases: pneumonia, viral research abstracts see: virus diseases: pneumonia, viral research

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IL-18, but not IL-12, regulates NK cell activity following intranasal herpes simplex virus type 1 infection. Journal Published:

PUBLICATION TYPE: Research Support, Non-U.S. Gov

Journal: Journal of immunology (Baltimore, Md. : 1950)

VOLUME: 179

Page Numbers: 3214-21

Journal Abbreviation: J. Immunol.

ISSN: 0022-1767

DAY: 1

MONTH: Sep

YEAR: 2007

IL-18, but not IL-12, regulates NK cell activity following intranasal herpes simplex virus type 1 infection. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 2985117

IL-18, but not IL-12, regulates NK cell activity following intranasal herpes simplex virus type 1 infection. Keywords Mesh Terms:

KEYWORDS: Pneumonia, Viral

MESH TERMS: immunology

Chemical & Substance for Abstract: IL-18, but not IL-12, regulates NK cell activity following intranasal herpes simplex virus type 1 infection. Information

Substance Name: Interleukin-12

Registry Number: 187348-17-0

Grant and Affiliation Information for IL-18, but not IL-12, regulates NK cell activity following intranasal herpes simplex virus type 1 infection.

AFFILIATION: Department of Microbiology and Immunology, The University of Melbourne, Parkville, Victoria 3010, Australia. preading@unimelb.edu.au

Country: United States

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MEDLINETA: J Immunol

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