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The host defense peptide cathelicidin is required for NK cell-mediated suppression of tumor growth.

Publication ,  Journal Article
Büchau, AS; Morizane, S; Trowbridge, J; Schauber, J; Kotol, P; Bui, JD; Gallo, RL
Published in: J Immunol
January 1, 2010

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.

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Published In

J Immunol

DOI

EISSN

1550-6606

Publication Date

January 1, 2010

Volume

184

Issue

1

Start / End Page

369 / 378

Location

United States

Related Subject Headings

  • Xenograft Model Antitumor Assays
  • Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization
  • Reverse Transcriptase Polymerase Chain Reaction
  • Mice, Knockout
  • Mice
  • Melanoma, Experimental
  • Killer Cells, Natural
  • Immunology
  • Immunologic Surveillance
  • Immunohistochemistry
 

Citation

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Büchau, A. S., Morizane, S., Trowbridge, J., Schauber, J., Kotol, P., Bui, J. D., & Gallo, R. L. (2010). The host defense peptide cathelicidin is required for NK cell-mediated suppression of tumor growth. J Immunol, 184(1), 369–378. https://doi.org/10.4049/jimmunol.0902110
Büchau, Amanda S., Shin Morizane, Janet Trowbridge, Jürgen Schauber, Paul Kotol, Jack D. Bui, and Richard L. Gallo. “The host defense peptide cathelicidin is required for NK cell-mediated suppression of tumor growth.J Immunol 184, no. 1 (January 1, 2010): 369–78. https://doi.org/10.4049/jimmunol.0902110.
Büchau AS, Morizane S, Trowbridge J, Schauber J, Kotol P, Bui JD, et al. The host defense peptide cathelicidin is required for NK cell-mediated suppression of tumor growth. J Immunol. 2010 Jan 1;184(1):369–78.
Büchau, Amanda S., et al. “The host defense peptide cathelicidin is required for NK cell-mediated suppression of tumor growth.J Immunol, vol. 184, no. 1, Jan. 2010, pp. 369–78. Pubmed, doi:10.4049/jimmunol.0902110.
Büchau AS, Morizane S, Trowbridge J, Schauber J, Kotol P, Bui JD, Gallo RL. The host defense peptide cathelicidin is required for NK cell-mediated suppression of tumor growth. J Immunol. 2010 Jan 1;184(1):369–378.

Published In

J Immunol

DOI

EISSN

1550-6606

Publication Date

January 1, 2010

Volume

184

Issue

1

Start / End Page

369 / 378

Location

United States

Related Subject Headings

  • Xenograft Model Antitumor Assays
  • Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization
  • Reverse Transcriptase Polymerase Chain Reaction
  • Mice, Knockout
  • Mice
  • Melanoma, Experimental
  • Killer Cells, Natural
  • Immunology
  • Immunologic Surveillance
  • Immunohistochemistry