The collagen binding alpha1beta1 integrin VLA-1 regulates CD8 T cell-mediated immune protection against heterologous influenza infection

Immunity. 2004 Feb;20(2):167-79. doi: 10.1016/s1074-7613(04)00021-4.


A common feature of many infections is that many pathogen-specific memory T cells become established in diverse nonlymphoid tissues. A mechanism that promotes the retention and survival of the memory T cells in diverse tissues has not been described. Our studies show that the collagen binding alpha1beta1 integrin, VLA-1, is expressed by the majority of influenza-specific CD8 T cells recovered from nonlymphoid tissues during both the acute and memory phases of the response. Antibody treatment or genetic deficiency of VLA-1 decreased virus-specific CTL in the lung and other nonlymphoid tissues, and increased them in the spleen. In spite of the increase in the spleen, secondary heterosubtypic immunity against flu was compromised. This suggests that VLA-1 is responsible for retaining protective memory CD8 T cells in the lung and other tissues via attachment to the extracellular matrix.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Apoptosis / immunology
  • CD8-Positive T-Lymphocytes / immunology*
  • CD8-Positive T-Lymphocytes / virology
  • Cell Adhesion / immunology
  • Collagen / immunology*
  • Collagen / metabolism
  • Female
  • Flow Cytometry
  • Immunocompetence
  • Immunohistochemistry
  • Immunologic Memory
  • In Situ Nick-End Labeling
  • Integrin alpha1beta1 / immunology*
  • Lung / immunology
  • Lung / pathology
  • Lung / virology
  • Lymphocyte Activation / immunology
  • Mice
  • Orthomyxoviridae Infections / immunology*
  • Spleen / immunology
  • Spleen / virology


  • Integrin alpha1beta1
  • Collagen