The Journal of Experimental Medicine
Avanti Polar Lipids
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Published online 14 April 2003 doi:10.1084/jem.20021047
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© Rockefeller University Press, 0022-1007/2003/4/1017 $5.00
The Journal of Experimental Medicine, Volume 197, Number 8, 1017-1028

Immune Enhancement of Skin Carcinogenesis by CD4+ T Cells

Dylan Daniel1, Nicole Meyer-Morse1, Emily K. Bergsland2, Kerstin Dehne3, Lisa M. Coussens3 and Douglas Hanahan1

1 Department of Biochemistry and Biophysics, Diabetes and Comprehensive Cancer Centers
2 Division of Hematology/Oncology, Department of Medicine
3 Cancer Research Institute, Department of Pathology, Comprehensive Cancer Center, University of California at San Francisco, San Francisco, CA 94143

Address correspondence to Douglas Hanahan, Diabetes Center, 513 Parnassus Ave., HSW 1090, University of California, San Francisco, San Francisco, CA 94143-0534. Phone: 415-476-9209; Fax: 415-731-3612; E-mail: dh{at}biochem.ucsf.edu

In a transgenic model of multi-stage squamous carcinogenesis induced by human papillomavirus (HPV) oncogenes, infiltrating CD4+ T cells can be detected in both premalignant and malignant lesions. The lymph nodes that drain sites of epidermal neoplasia contain activated CD4+ T cells predominantly reactive toward Staphylococcal bacterial antigens. HPV16 mice deficient in CD4+ T cells were found to have delayed neoplastic progression and a lower incidence of tumors. This delay in carcinogenesis is marked by decreased infiltration of neutrophils, and reduced activity of matrix metalloproteinase-9, an important cofactor for tumor progression in this model. The data reveal an unexpected capability of CD4 T cells, whereby, proinflammatory CD4+ T cells, apparently responding to bacterial infection of dysplastic skin lesions, can inadvertently enhance neoplastic progression to invasive cancer.

Key Words: mice • transgenic • cancer • inflammation • lymphocyte


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