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

Authors
  • Beura, Lalit K
  • Anderson, Kristin G
  • Schenkel, Jason M
  • Locquiao, Jeremiah J
  • Fraser, Kathryn A
  • Vezys, Vaiva
  • Pepper, Marion
  • Masopust, David
Type
Published Article
Journal
Journal of Leukocyte Biology
Publisher
Wiley (John Wiley & Sons)
Publication Date
Feb 01, 2015
Volume
97
Issue
2
Pages
217–225
Identifiers
DOI: 10.1189/jlb.1HI0314-154R
PMID: 25395301
Source
Medline
Keywords
License
Unknown

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.

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