Minimal effect of CD103 expression on the control of a chronic antiviral immune response

Georgia Fousteri, Amy Dave, Therese Juntti, Bret Morin, Malina McClure, Matthias Von Herrath

Research output: Contribution to journalArticlepeer-review


Impaired antiviral CD8 and CD4 T-cell responses are often associated with chronic viral infections. Cell-intrinsic as well as cell-extrinsic mechanisms are thought to dampen such responses, for example programmed death 1 receptor (PD-1) expression on T cells, and interleukin (IL)-10 production primarily by dendritic cells (DCs), have been shown to support viral persistence by suppressing immune responses. Here we demonstrate that CD103, an alpha E integrin necessary for T-cell homing and retention in the gut and other epithelia expressed by the majority of naïve CD8+, and CD4 +CD25+ T cells and some DC subsets, is unnecessary for controlling T-cell responses during chronic lymphocytic choriomeningitis virus clone 13 (LCMV cl13) infection. T-cell analysis following viral infection showed that the primary as well as the memory CD8+ and CD4+ T-cell responses among CD103-sufficient and CD103-deficient mice were identical. In addition, no rescue of cytokine production by virus-specific T cells or alterations in viral titers in the absence of intrinsic CD103 expression was observed. Interestingly, CD103 levels on the effector CD8+ T cells became reduced soon after virus infection, with a small proportion of cells co-expressing PD-1 and CD103. In contrast, although no substantial differences in the frequency and number of the CD4+CD25+ cell population were seen, CD103 expression increased significantly over time in this population, correlating with viral persistence. Thus, a lack of CD103 expression does not affect functional impairment of effector T-cell responses during chronic viral infection.

Original languageEnglish
Pages (from-to)285-294
Number of pages10
JournalViral Immunology
Issue number3
Publication statusPublished - Jun 1 2010

ASJC Scopus subject areas

  • Immunology
  • Virology
  • Molecular Medicine


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