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NKG2D-dependent effector function of bronchial epithelium-activated alloreactive T-cells

Depts of ¹ Internal Medicine II, and ² Hematology and Oncology, University of Regensburg, Regensburg, and ³ Dept of Radiotherapy and Radiooncology, Klinkum rechts der Isar, Munich Technical University, Munich, Germany, ⁴ Both authors contributed equally.

CORRESPONDENCE: C. Schulz, Dept of Internal Medicine II, University of Regensburg, Franz-Josef-Strauss-Allee 11, Regensburg, 93053 Germany. Fax: 49 94194407282. E-mail: christian.schulz{at}klinik.uni-regensburg.de

Keywords: Alloreaction, CD8 T-cells, lung, major histocompatibility complex I, natural killer group 2 member D

Received: July 29, 2007
Accepted April 7, 2008

Allogeneic haematopoietic stem cell transplantation (SCT) has emerged as a curative therapeutic option. However, the role of graft-versus-host disease in lung injury after SCT has yet to be determined.

In the present study, primary bronchial epithelial cells and the bronchial epithelial cell line BEAS-2B were used to investigate immune responses of allogeneic CD8+ T-cells directed against respiratory epithelial cells.

Following stimulation with irradiated bronchial epithelial cells, CD8+ T-cells produced significant amounts of interferon-, upregulated alloantigen activation markers and proliferated highly compared with T-cells stimulated with interleukin-2 alone. Furthermore, cytotoxicity assays demonstrated that bronchial epithelial cell-specific and granzyme B-mediated cytolytic activity was induced in CD8+ T-cells. Generation of natural killer (NK) T-cells, NK-like T-cells, cytokine-induced killer cells or lymphokine-activated killer cells could be excluded by phenotyping, culture conditions and neglectable lytic activity following stimulation with interleukin-2 alone. Inhibition experiments showed that lysis of bronchial epithelial cells was not major histocompatibility complex-I restricted, but depended on NK group 2 member D signalling; a stimulatory receptor initially shown to be expressed on NK cells.

The present data imply that the respiratory epithelium has an antigen presenting function and directly alloactivates cytotoxic CD8+ T-cells that show nonclassical effector function.