Allergen exposure functionally alters influenza-specific CD4+ Th1 memory cells in the lung.

Autor:	Rüterbusch MJ; Department of Immunology, School of Medicine, University of Washington, Seattle, WA, USA., Hondowicz BD; Department of Immunology, School of Medicine, University of Washington, Seattle, WA, USA., Takehara KK; Department of Immunology, School of Medicine, University of Washington, Seattle, WA, USA., Pruner KB; Department of Immunology, School of Medicine, University of Washington, Seattle, WA, USA., Griffith TS; Department of Urology, University of Minnesota, Minneapolis, MN, USA.; Microbiology, Immunology, and Cancer Biology Ph.D. Program, University of Minnesota , Minneapolis, MN, USA.; Center for Immunology, University of Minnesota , Minneapolis, MN, USA.; Masonic Cancer Center, University of Minnesota , Minneapolis, MN, USA., Pepper M; Department of Immunology, School of Medicine, University of Washington, Seattle, WA, USA.
Jazyk:	angličtina
Zdroj:	The Journal of experimental medicine [J Exp Med] 2023 Nov 06; Vol. 220 (11). Date of Electronic Publication: 2023 Sep 12.
DOI:	10.1084/jem.20230112
Abstrakt:	CD4+ lung-resident memory T cells (TRM) generated in response to influenza infection confer effective protection against subsequent viral exposures. Whether these cells can be altered by environmental antigens and cytokines released during heterologous, antigen-independent immune responses is currently unclear. We therefore investigated how influenza-specific CD4+ Th1 TRM in the lung are impacted by a subsequent Th2-inducing respiratory house dust mite (HDM) exposure. Although naïve influenza-specific CD4+ T cells in the lymph nodes do not respond to HDM, influenza-specific CD4+ TRM in the lungs do respond to a subsequent allergen exposure by decreasing expression of the transcription factor T-bet. This functional alteration is associated with decreased IFN-γ production upon restimulation and improved disease outcomes following heterosubtypic influenza challenge. Further investigation revealed that ST2 signaling in CD4+ T cells during allergic challenge is necessary to induce these changes in lung-resident influenza-specific CD4+ TRM. Thus, heterologous antigen exposure or ST2-signaling can drive persistent changes in CD4+ Th1 TRM populations and impact protection upon reinfection. (© 2023 Rüterbusch et al.)
Databáze:	MEDLINE
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