Interleukin 2-mediated conversion of ovarian cancer-associated CD4+ regulatory T cells into proinflammatory interleukin 17-producing helper T cells.
Leveque L, Deknuydt F, Bioley G, Old LJ, Matsuzaki J, Odunsi K, Ayyoub M, Valmori D.
J Immunother. 2009 Feb-Mar;32(2):101-8.
PMID: 19238008
doi: 10.1097/CJI.0b013e318195b59e
Thus, although the impact of TH17 cells on the evolution of EOC remains to be established, our data suggest that local IL-2 treatment in ovarian cancer may result in the conversion of tumor-associated Treg into TH17 cells, relieve Treg-mediated suppression, and contribute to enhance antitumor immunity.
Th1/Th2 balance: the hypothesis, its limitations, and implications for health and disease.
Kidd P.
Altern Med Rev. 2003 Aug;8(3):223-46. Review.
PMID: 12946237
Th1 pathways typically produce activation
of cytotoxic T lymphocytes (Tc), NK cells,
macrophages, and monocytes, all of which can
attack cancer cells and generally defend against
tumors.55 IFN-gamma and other Th1 cytokines are
typically lower in advanced cancer patients, while
the Th2 marker IL-4 can be higher or unchanged
Preoperative treatment with a non-steroidal anti-inflammatory drug (NSAID) increases tumor tissue infiltration of seemingly activated immune cells in colorectal cancer.
Lönnroth C, Andersson M, Arvidsson A, Nordgren S, Brevinge H, Lagerstedt K, Lundholm K.
Cancer Immun. 2008 Feb 29;8:5.
PMID: 18307280
MHC II protein (HLA-DP, -DQ, -DR) levels and infiltration by CD4+ T-helper cells of tumor stroma increased upon NSAID treatment, while CD8+ cytotoxic T-lymphocytes increased in both tumor stroma and epithelium. Molecules associated with immunosuppressive T regulatory cells (FOXP3, IL-10) were significantly decreased in indomethacin-exposed tumors. Standard oral administration of NSAID three days preoperatively was enough to increase tumor infiltration by seemingly activated immune cells. These findings agree with previous information that high pr