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Identification of a unique population of tissue-memory CD4+ T cells in the airways after influenza infection that is dependent on the integrin VLA-1.

Abstract
During the immune response to influenza infection, activated T cells are distributed to both lymphoid and extralymphoid tissues, including the infected airways where direct recognition of viral Ag-bearing cells takes place. The collagen-binding alpha(1)beta(1) integrin VLA-1 is essential for the development of memory CD8(+) T cells in the airways, and although expressed by some CD4(+) T cells, its significance has not been demonstrated. We investigated the role of VLA-1 on virus-specific CD4(+) T cells during and after primary or secondary influenza infection of mice. The proportion of CD4(+) cells expressing CD49a (alpha(1) integrin) was low in all tissues sampled during primary infection but increased in the airways after viral clearance. Furthermore, during the first 24 h of a secondary influenza challenge, the majority of IFN-gamma-secreting effector CD4(+) T cells from the airways was in the CD49a(+) population. Airway CD49a(+)CD4(+) cells also expressed reduced markers of apoptosis compared with CD49a(-) cells, and fewer memory or effector CD4(+) cells could be recovered from airways of alpha(1)(-/-) mice, although lymphoid tissues appeared unaffected. These data suggest VLA-1 expression defines a population of tissue memory CD4(+) T cells that act as rapid effectors upon reinfection, and VLA-1 expression is integral to their accumulation in the airways.
AuthorsTimothy J Chapman, David J Topham
JournalJournal of immunology (Baltimore, Md. : 1950) (J Immunol) Vol. 184 Issue 7 Pg. 3841-9 (Apr 01 2010) ISSN: 1550-6606 [Electronic] United States
PMID20200271 (Publication Type: Journal Article, Research Support, N.I.H., Extramural)
Chemical References
  • Integrin alpha1beta1
Topics
  • Animals
  • CD4-Positive T-Lymphocytes (immunology)
  • Cell Separation
  • Flow Cytometry
  • Immunologic Memory
  • Influenza A virus (immunology)
  • Integrin alpha1beta1 (immunology)
  • Lung (immunology, virology)
  • Lymphocyte Activation (immunology)
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Orthomyxoviridae Infections (immunology)
  • T-Lymphocyte Subsets (immunology)

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