Antigen-Induced but Not Innate Memory CD8 T Cells Express NKG2D and Are Recruited to the Lung Parenchyma upon Viral Infection | Zendy

Morgan Grau | Zendy; Séverine Valsesia | Zendy; Julien Mafille | Zendy; Sophia Djebali | Zendy; Martine Tomkowiak | Zendy; AnneLaure Mathieu | Zendy; Daphné Laubreton | Zendy; Simon de Bernard | Zendy; P Jouve | Zendy; Erwan Ventre | Zendy; Laurent Buffat | Zendy; Thierry Walzer | Zendy; Yann Leverrier | Zendy; Jacqueline Marvel | Zendy

Open Access

Antigen-Induced but Not Innate Memory CD8 T Cells Express NKG2D and Are Recruited to the Lung Parenchyma upon Viral Infection

Author(s) -

Morgan Grau,

Séverine Valsesia,

Julien Mafille,

Sophia Djebali,

Martine Tomkowiak,

AnneLaure Mathieu,

Daphné Laubreton,

Simon de Bernard,

P Jouve,

Erwan Ventre,

Laurent Buffat,

Thierry Walzer,

Yann Leverrier,

Jacqueline Marvel

Publication year - 2018

Publication title -

the journal of immunology

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 2.737

H-Index - 372

eISSN - 1550-6606

pISSN - 0022-1767

DOI - 10.4049/jimmunol.1701698

Subject(s) - parenchyma , innate immune system , nkg2d , immunology , virology , lung , antigen , cd8 , cytotoxic t cell , viral infection , biology , virus , medicine , pathology , immune system , biochemistry , in vitro

The pool of memory-phenotype CD8 T cells is composed of Ag-induced (AI) and cytokine-induced innate (IN) cells. IN cells have been described as having properties similar to those of AI memory cells. However, we found that pathogen-induced AI memory cells can be distinguished in mice from naturally generated IN memory cells by surface expression of NKG2D. Using this marker, we described the increased functionalities of AI and IN memory CD8 T cells compared with naive cells, as shown by comprehensive analysis of cytokine secretion and gene expression. However, AI differed from IN memory CD8 T cells by their capacity to migrate to the lung parenchyma upon inflammation or infection, a process dependent on their expression of ITGA1/CD49a and ITGA4/CD49d integrins.

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