NDLI: KLRG1+ NK cells protect T-bet-deficient mice from pulmonary metastatic colorectal carcinoma.

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KLRG1+ NK cells protect T-bet-deficient mice from pulmonary metastatic colorectal carcinoma.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Schlitt, Hans J. Sabet-Baktach, Manije Eggenhofer, Elke Malaisé, Muriel Lang, Sven A. Farkas, Stefan A. Koehl, Gudrun E. Geissler, Edward K. Lantow, Margareta Rovira, Jordi Agha, Ayman Kroemer, Alexander Renner, Philipp Loss, Martin Campistol, Josep M.
Description	Country affiliation: Germany Author Affiliation: Malaisé M ( Department of Surgery, University Hospital Regensburg, 93053 Regensburg, Germany.)
Abstract	We studied the developmental and functional mechanisms behind NK cell-mediated antitumor responses against metastatic colorectal carcinoma (CRC) in mice. In particular, we focused on investigating the significance of T-box transcription factors and the immunotherapeutic relevance of IL-15 in the development and function of tumor-reactive NK cells. Pulmonary CRC metastases were experimentally seeded via an adoptive i.v. transfer of luciferase-expressing CT26 CRC cells that form viewable masses via an in vivo imaging device; genetically deficient mice were used to dissect the antitumor effects of developmentally different NK cell subsets. IL-15 precomplexed to IL-15 receptor- was used in immunotherapy experiments. We found that mice deficient for the T-box transcription factor T-bet lack terminally differentiated antitumor CD27(low)KLRG1(+) NK cells, leading to a terminal course of rapid-onset pulmonary CRC metastases. The importance of this NK cell subset for effective antitumor immunity was shown by adoptively transferring purified CD27(low)KLRG1(+) NK cells into T-bet-deficient mice and, thereby, restoring immunity against lung metastasis formation. Importantly, immunity to metastasis formation could also be restored in T-bet-deficient recipients by treating mice with IL-15 precomplexed to IL-15 receptor- , which induced the development of eomesodermin(+)KLRG1(+) NK cells from existing NK cell populations. Thus, contingent upon their T-bet-dependent development and activation status, NK cells can control metastatic CRC in mice, which is highly relevant for the development of immunotherapeutic approaches in the clinic.
ISSN	00221767
e-ISSN	15506606
Journal	The Journal of Immunology
Issue Number	4
Volume Number	192
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2014-02-15
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Colorectal Neoplasms Pathology Killer Cells, Natural Immunology Lung Neoplasms Receptors, Immunologic Metabolism T-box Domain Proteins Genetics Adoptive Transfer Animals Antigens, Cd27 Cell Differentiation Cells, Cultured Therapy Homeodomain Proteins Immunotherapy Interferon-gamma Interleukin-15 Cytology Prevention & Control Mice Mice, Inbred Balb C Mice, Knockout Perforin Pore Forming Cytotoxic Proteins Receptors, Interleukin-15 Recombinant Fusion Proteins Therapeutic Use Deficiency Research Support, Non-u.s. Gov't Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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