title: New strategies for the manipulation of adaptive immune responses.
abstract: The maintenance of peripheral tolerance is largely based on thymus-derived CD4(+)CD25(+) naturally occurring regulatory T cells (Tregs). While on the one hand being indispensable for the perpetuation of tolerance to self-antigens, the immune suppressive properties of Tregs contribute to cancer pathogenesis and progression. Thus, modulation of Treg function represents a promising strategy to support tumor eradication in immunotherapy of cancer. Here, we discuss potential therapeutic applications of our observation that Tregs contain high concentrations of the second messenger cyclic adenosine monophosphate, which is transferred from Tregs via gap junctions to suppress the function of T cells and dendritic cells.
authors.affiliation: Institute for Immunology, University Medical Centre of the Johannes Gutenberg-University Mainz, Mainz, Germany.
authors.forename: Tobias
authors.initials: T
authors.lastname: Bopp
authors.forename: Markus
authors.initials: M
authors.lastname: Radsak
authors.forename: Edgar
authors.initials: E
authors.lastname: Schmitt
authors.forename: Hansjörg
authors.initials: H
authors.lastname: Schild
mesh_terms: D056704:Adaptive Immunity; D000818:Animals; D000970:Antineoplastic Agents / Q000494:pharmacology; D000242:Cyclic AMP / Q000276:immunology*; D017629:Gap Junctions; D006801:Humans; D007108:Immune Tolerance; D056747:Immunomodulation; D008212:Lymphocyte Depletion; D009369:Neoplasms / Q000276:immunology* / Q000628:therapy; D058988:Phosphodiesterase 4 Inhibitors; D050378:T-Lymphocytes, Regulatory / Q000276:immunology*
chemical_list: D000970:Antineoplastic Agents; D058988:Phosphodiesterase 4 Inhibitors; D000242:Cyclic AMP