Please use this identifier to cite or link to this item:
Scopus Web of Science® Altmetric
Type: Journal article
Title: SOCS4 is dispensable for an efficient recall response to influenza despite being required for primary immunity
Author: Kedzierski, L.
Clemens, E.B.
Bird, N.L.
Kile, B.T.
Belz, G.T.
Nicola, N.A.
Kedzierska, K.
Nicholson, S.E.
Citation: Immunology and Cell Biology, 2015; 93(10):909-913
Publisher: Nature Publishing Group
Issue Date: 2015
ISSN: 0818-9641
Statement of
Lukasz Kedzierski, E Bridie Clemens, Nicola L Bird, Benjamin T Kile, Gabrielle T Belz, Nicos A Nicola, Katherine Kedzierska, Sandra E Nicholson
Abstract: Suppressor of cytokine signaling (SOCS) proteins are key regulators of innate and adaptive immunity. Mice lacking functional SOCS4 are hypersusceptible to primary infection with influenza A virus (IAV), displaying dysregulated pro-inflammatory cytokine and chemokine production in the lungs, delayed viral clearance and impaired trafficking of influenza-specific CD8(+) T cells to the site of infection. Therefore, we postulated that SOCS4 is a critical regulator of anti-viral immunity. Unexpectedly, SOCS4 was not required for CD8(+) T-cell memory generation, nor was it required to efficiently recall those cells in response to secondary IAV infection. Wild-type or SOCS4-deficient mice primed and re-challenged with serologically different influenza strains, did not show differences in susceptibility to IAV and cleared the virus from the lungs at the same rate. We have not observed differences in trafficking or numbers of IAV-specific cells, numbers of resident memory T cells or in cytokine profiles in lungs of infected animals. Our data show that despite an impaired primary immune response in Socs4(R108X/R108X) mice, SOCS4 is dispensable for an efficient recall response to influenza virus infection.
Keywords: CD8-Positive T-Lymphocytes
Rights: © 2015 Australasian Society for Immunology Inc.
DOI: 10.1038/icb.2015.55
Grant ID:
Published version:
Appears in Collections:Aurora harvest 8
Medicine publications

Files in This Item:
There are no files associated with this item.

Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.