Sara D Johnson1, Corinne Levingston2, M Rita I Young3. 1. Research Service (151) Ralph H. Johnson Veterans Affairs Medical Center, Charleston, SC, U.S.A. Department of Pathology and Laboratory Medicine, Medical University of South Carolina, Charleston, SC, U.S.A. Department of Otolaryngology-Head and Neck Surgery, Medical University of South Carolina, Charleston, SC, U.S.A. 2. Research Service (151) Ralph H. Johnson Veterans Affairs Medical Center, Charleston, SC, U.S.A. 3. Research Service (151) Ralph H. Johnson Veterans Affairs Medical Center, Charleston, SC, U.S.A. Department of Otolaryngology-Head and Neck Surgery, Medical University of South Carolina, Charleston, SC, U.S.A. Department of Medicine, Medical University of South Carolina, Charleston, SC, U.S.A. rita.young@va.gov.
Abstract
BACKGROUND: Head and neck squamous cell carcinomas (HNSCC) are known to evade the host immune response. How premalignant oral lesions modulate the immune response, however, has yet to be elucidated. MATERIALS AND METHODS: A mouse model of oral carcinogenesis was used to determine how mediators from premalignant oral lesion cells vs. HNSCC cells impact on immune cytokine production and activation. RESULTS: Media conditioned by premalignant lesion cells elicited an increased production of T cell-associated cytokines and proinflammatory mediators from cervical lymph node cells compared to media conditioned by HNSCC cells or media alone. In the presence of premalignant lesion cell-conditioned media, CD4(+) T cell expression of the IL-2 receptor CD25 and CD8(+) T cell expression of the activation marker CD69 was greater, compared to what was induced in HNSCC cell-conditioned media or media alone. CONCLUSION: Premalignant lesion cells promote a proinflammatory environment and induce immune changes before HNSCC tumors are established. Copyright
BACKGROUND: Head and neck squamous cell carcinomas (HNSCC) are known to evade the host immune response. How premalignant oral lesions modulate the immune response, however, has yet to be elucidated. MATERIALS AND METHODS: A mouse model of oral carcinogenesis was used to determine how mediators from premalignant oral lesion cells vs. HNSCC cells impact on immune cytokine production and activation. RESULTS: Media conditioned by premalignant lesion cells elicited an increased production of T cell-associated cytokines and proinflammatory mediators from cervical lymph node cells compared to media conditioned by HNSCC cells or media alone. In the presence of premalignant lesion cell-conditioned media, CD4(+) T cell expression of the IL-2 receptor CD25 and CD8(+) T cell expression of the activation marker CD69 was greater, compared to what was induced in HNSCC cell-conditioned media or media alone. CONCLUSION:Premalignant lesion cells promote a proinflammatory environment and induce immune changes before HNSCC tumors are established. Copyright
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