期刊
JOURNAL OF IMMUNOLOGY
卷 184, 期 1, 页码 369-378出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.0902110
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资金
- Veterans Affairs merit award
- National Institutes of Health [A1052453, AR45676, CA128893]
- American Cancer Society
- Cancer Research Coordinating Committee
- V Foundation
- Concern Foundation
- Deutsche Akademie der Naturforscher Leopoldina [BMBF-LPD 9901/8-119]
- Deutsche Forschungsgemeinschaft [BU 2212/1-1]
- NATIONAL CANCER INSTITUTE [K08CA128893] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [R01AI052453, R37AI052453] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN DISEASES [R01AR045676] Funding Source: NIH RePORTER
Tumor surveillance requires the interaction of multiple molecules and cells that participate in innate and the adaptive immunity. Cathelicidin was initially identified as an antimicrobial peptide, although it is now clear that it fulfills a variety of immune functions beyond microbial killing. Recent data have suggested contrasting roles for cathelicidin in tumor development. Because its role in tumor surveillance is not well understood, we investigated the requirement of cathelicidin in controlling transplantable tumors in mice. Cathelicidin was observed to be abundant in tumor-infiltrating NK1.1(+) cells in mice. The importance of this finding was demonstrated by the fact that cathelicidin knockout mice (Camp(-/-)) permitted faster tumor growth than wild type controls in two different xenograft tumor mouse models (B16.F10 and RMA-S). Functional in vitro analyses found that NK cells derived from Camp(-/-) versus wild type mice showed impaired cytotoxic activity toward tumor targets. These findings could not be solely attributed to an observed perforin deficiency in freshly isolated Camp(-/-) NK cells, because this deficiency could be partially restored by IL-2 treatment, whereas cytotoxic activity was still defective in IL-2-activated Camp(-/-) NK cells. Thus, we demonstrate a previously unrecognized role of cathelicidin in NK cell antitumor function. The Journal of Immunology, 2010, 184: 369-378.
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