Journal article

SOCS4 is dispensable for an efficient recall response to influenza despite being required for primary immunity

Lukasz Kedzierski, E Bridie Clemens, Nicola L Bird, Benjamin T Kile, Gabrielle T Belz, Nicos A Nicola, Katherine Kedzierska, Sandra E Nicholson

IMMUNOLOGY AND CELL BIOLOGY | NATURE PUBLISHING GROUP | Published : 2015

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..

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Grants

Awarded by National Health and Medical Research Council (NHMRC), Australia


Awarded by NHMRC IRIISS grant


Awarded by National Institutes of Health


Awarded by NATIONAL CANCER INSTITUTE


Funding Acknowledgements

We thank Sarah Freeman for technical assistance and Liana Mackiewicz for excellent animal husbandry. This work was supported in part by the National Health and Medical Research Council (NHMRC), Australia (Program grant number 1016647, Project grant APP1023559), as well as an NHMRC IRIISS grant 361646 and a Victorian State Government Operational Infrastructure Scheme grant. KK is a recipient of an NHMRC CDA2 Fellowship, SEN, BTK and NAN were supported by NHMRC fellowships, GTB is a recipient of an Australian Research Council Fellowship. This work was also supported in part by the National Institutes of Health (5R37CA022556).