Lymphocytic choriomeningitis virus persistence promotes effector-like memory differentiation and enhances mucosal T cell distribution

Lalit K. Beura, Kristin G. Anderson, Jason M. Schenkel, Jeremiah J. Locquiao, Kathryn A. Fraser, Vaiva Vezys, Marion Pepper, David Masopust

Research output: Contribution to journalArticlepeer-review

31 Scopus citations

Abstract

Vaccines are desired that maintain abundant memory T cells at nonlymphoid sites of microbial exposure, where they may be anatomically positioned for immediate pathogen interception. Here, we test the impact of antigen persistence on mouse CD8 and CD4 T cell distribution and differentiation by comparing responses to infections with different strains of LCMV that cause either acute or chronic infections. We used in vivo labeling techniques that discriminate between T cells present within tissues and abundant populations that fail to be removed from vascular compartments, despite perfusion. LCMV persistence caused up to ~30-fold more virus-specific CD8 T cells to distribute to the lung compared with acute infection. Persistent infection also maintained mucosal-homing α4β7 integrin expression, higher granzyme B expression, alterations in the expression of the TRM markers CD69 and CD103, and greater accumulation of virus-specific CD8 T cells in the large intestine, liver, kidney, and female reproductive tract. Persistent infection also increased LCMV-specific CD4 T cell quantity in mucosal tissues and induced maintenance of CXCR4, an HIV coreceptor. This study clarifies the relationship between viral persistence and CD4 and CD8 T cell distribution and mucosal phenotype, indicating that chronic LCMV infection magnifies T cell migration to nonlymphoid tissues.

Original languageEnglish (US)
Pages (from-to)217-225
Number of pages9
JournalJournal of Leukocyte Biology
Volume97
Issue number2
DOIs
StatePublished - Feb 1 2015

Bibliographical note

Publisher Copyright:
© Society for Leukocyte Biology.

Keywords

  • CD8 T cells
  • Homing

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