IL-23 orchestrates the switch from tumor immune surveillance to tumor-promoting inflammation
Human tumor cells acquire and accumulate mutations and transcriptional changes that provide growth and survival signals and a tumor-promoting microenvironment. Over the last few decades it has become clear that the mammalian immune system is able to recognize these genetic and epigenetic changes, and that T cells specific to oncogenes and oncofetal antigens are present in human cancer patients and their tumors. Immune-mediated inflammation, however, increases tumor incidence and progression. Epidemiologically, inflammatory disease-inducing cytokines have also been linked to tumor progression. However, the nature of the pro-inflammatory T cells that control the chronic inflammatory response, and their regulation by cytokines like IL-23, only became known recently. This review attempts to summarize our knowledge of pro-inflammatory T cells in cancer, and the cytokines that contribute to the deregulation of tumor-promoting inflammation and its inhibitory consequences on the tumor cell elimination by cytotoxic T cells.
KeywordsImmune Surveillance Cytokine Milieu Oncofetal Antigen Human Cancer Patient Mammalian Immune System
Unable to display preview. Download preview PDF.
- 13.Rosenberg SA, Sherry RM, Morton KE, Scharfman WJ, Yang JC, Topalian SL, Royal RE, Kammula U, Restifo NP, Hughes MS et al (2005) Tumor progression can occur despite the induction of very high levels of self/tumor antigen-specific CD8+ T cells in patients with melanoma. J Immunol 175: 6169–6176PubMedGoogle Scholar
- 46.Chan JR, Blumenschein W, Murphy E, Diveu C, Wiekowski M, Abbondanzo S, Lucian L, Geissler R, Brodie S, Kimball AB et al (2006) IL-23 stimulates epidermal hyperplasia via TNF and IL-20R2-dependent mechanisms with implications for psoriasis pathogenesis. J Exp Med 203: 2577–2587PubMedCrossRefGoogle Scholar