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

Research output: Contribution to journalArticleResearchpeer-review

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 Socs4R108X/R108X mice, SOCS4 is dispensable for an efficient recall response to influenza virus infection.

Original languageEnglish
Pages (from-to)909-913
Number of pages5
JournalImmunology and Cell Biology
Volume93
Issue number10
DOIs
Publication statusPublished - Nov 2015
Externally publishedYes

Cite this

Kedzierski, Lukasz ; Clemens, E Bridie ; Bird, Nicola L ; Kile, Benjamin T ; Belz, Gabrielle T ; Nicola, Nicos A ; Kedzierska, Katherine ; Nicholson, Sandra E. / SOCS4 is dispensable for an efficient recall response to influenza despite being required for primary immunity. In: Immunology and Cell Biology. 2015 ; Vol. 93, No. 10. pp. 909-913.
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title = "SOCS4 is dispensable for an efficient recall response to influenza despite being required for primary immunity",
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 Socs4R108X/R108X mice, SOCS4 is dispensable for an efficient recall response to influenza virus infection.",
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Kedzierski, L, Clemens, EB, Bird, NL, Kile, BT, Belz, GT, Nicola, NA, Kedzierska, K & Nicholson, SE 2015, 'SOCS4 is dispensable for an efficient recall response to influenza despite being required for primary immunity' Immunology and Cell Biology, vol. 93, no. 10, pp. 909-913. https://doi.org/10.1038/icb.2015.55

SOCS4 is dispensable for an efficient recall response to influenza despite being required for primary immunity. / Kedzierski, Lukasz; Clemens, E Bridie; Bird, Nicola L; Kile, Benjamin T; Belz, Gabrielle T; Nicola, Nicos A; Kedzierska, Katherine; Nicholson, Sandra E.

In: Immunology and Cell Biology, Vol. 93, No. 10, 11.2015, p. 909-913.

Research output: Contribution to journalArticleResearchpeer-review

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AU - Kedzierski, Lukasz

AU - Clemens, E Bridie

AU - Bird, Nicola L

AU - Kile, Benjamin T

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AU - Kedzierska, Katherine

AU - Nicholson, Sandra E

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