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Enhanced resistance in STAT6-deficient mice to infection with ectromelia virus

Citation

Mahalingam, S and Karupiah, G and Takeda, K and Akira, S and Matthaei, KI and Foster, PS, Enhanced resistance in STAT6-deficient mice to infection with ectromelia virus, National Academy of Sciences of The United States of America. Proceedings, 98, (12) pp. 6812-6817. ISSN 0027-8424 (2001) [Refereed Article]

Copyright Statement

Copyright 2001 the authors

DOI: doi:10.1073/pnas.111151098

Abstract

We inoculated BALByc mice deficient in STAT6 (STAT62/2) and their wild-type (wt) littermates (STAT61/1) with the natural mouse pathogen, ectromelia virus (EV). STAT62/2 mice exhibited increased resistance to generalized infection with EV when compared with STAT61/1 mice. In the spleens and lymph nodes of STAT62/2 mice, T helper 1 (Th1) cytokines were induced at earlier time points and at higher levels postinfection when compared with those in STAT61/1 mice. Elevated levels of NO were evident in plasma and splenocyte cultures of EV-infected STAT62/2 mice in comparison with STAT61/1 mice. The induction of high levels of Th1 cytokines in the mutant mice correlated with a strong natural killer cell response. We demonstrate in genetically susceptible BALByc mice that the STAT6 locus is critical for progression of EV infection. Furthermore, in the absence of this transcription factor, the immune system defaults toward a protective Th1-like response, conferring pronounced resistance to EV infection and disease progression.

Item Details

Item Type:Refereed Article
Keywords:Th2 responses; Poxvirus immunity
Research Division:Biomedical and Clinical Sciences
Research Group:Immunology
Research Field:Cellular immunology
Objective Division:Health
Objective Group:Clinical health
Objective Field:Prevention of human diseases and conditions
UTAS Author:Karupiah, G (Associate Professor Guna Karupiah)
ID Code:142830
Year Published:2001
Web of Science® Times Cited:22
Deposited By:Medicine
Deposited On:2021-02-12
Last Modified:2021-09-22
Downloads:0

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