Abstract
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.
Original language | English (US) |
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Pages (from-to) | 1017-1028 |
Number of pages | 12 |
Journal | Journal of Experimental Medicine |
Volume | 197 |
Issue number | 8 |
DOIs | |
State | Published - Apr 21 2003 |
Externally published | Yes |
Keywords
- Cancer
- Inflammation
- Lymphocyte
- Mice
- Transgenic
ASJC Scopus subject areas
- Immunology and Allergy
- Immunology