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Mouse cytomegalovirus-experienced ILC1s acquire a memory response dependent on the viral glycoprotein m12.

  • Author(s): Weizman, Orr-El;
  • Song, Eric;
  • Adams, Nicholas M;
  • Hildreth, Andrew D;
  • Riggan, Luke;
  • Krishna, Chirag;
  • Aguilar, Oscar A;
  • Leslie, Christina S;
  • Carlyle, James R;
  • Sun, Joseph C;
  • O'Sullivan, Timothy E
  • et al.
Abstract

Innate lymphoid cells (ILCs) are tissue-resident sentinels that are essential for early host protection from pathogens at initial sites of infection. However, whether pathogen-derived antigens directly modulate the responses of tissue-resident ILCs has remained unclear. In the present study, it was found that liver-resident type 1 ILCs (ILC1s) expanded locally and persisted after the resolution of infection with mouse cytomegalovirus (MCMV). ILC1s acquired stable transcriptional, epigenetic and phenotypic changes a month after the resolution of MCMV infection, and showed an enhanced protective effector response to secondary challenge with MCMV consistent with a memory lymphocyte response. Memory ILC1 responses were dependent on the MCMV-encoded glycoprotein m12, and were independent of bystander activation by proinflammatory cytokines after heterologous infection. Thus, liver ILC1s acquire adaptive features in an MCMV-specific manner.

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