Proceedings of the National Academy of Sciences - PNAS, 2012-09, Vol.109 (38), p.15413-15418
2012
Details
- Autor(en) / Beteiligte
- Titel
- TIPE2 protein serves as a negative regulator of phagocytosis and oxidative burst during infection
- Ist Teil von
- Proceedings of the National Academy of Sciences - PNAS, 2012-09, Vol.109 (38), p.15413-15418
- Ort / Verlag
- United States: National Academy of Sciences
- Erscheinungsjahr
- 2012
- Link zum Volltext
- Quelle
- Free E-Journal (出版社公開部分のみ）
- Beschreibungen/Notizen
- Phagocytosis and oxidative burst are two major effector arms of innate immunity. Although it is known that both are activated by Toll-like receptors (TLRs) and Rac GTPases, how their strengths are controlled in quiescent and TLR-activated cells is not clear. We report here that TIPE2 (TNFAIP8L2) serves as a negative regulator of innate immunity by linking TLRs to Rac. TLRs control the expression levels of TIPE2, which in turn dictates the strengths of phagocytosis and oxidative burst by binding to and blocking Rac GTPases. Consequently, TIPE2 knockout cells have enhanced phagocytic and bactericidal activities and TIPE2 knockout mice are resistant to bacterial infection. Thus, TIPE2 sets the strengths of phagocytosis and oxidative burst and may be targeted to effectively control infections.
- Sprache
- Englisch
- Identifikatoren
- ISSN: 0027-8424eISSN: 1091-6490DOI: 10.1073/pnas.1204525109Titel-ID: cdi_proquest_miscellaneous_1041325944
- Format
- –
- Schlagworte
- Actins, Amino Acid Motifs, Animals, Bacteria, Bacterial infections, Binding sites, Biological Sciences, Cell Line, Cell Membrane - metabolism, Cellular immunity, Crosses, Genetic, Down regulation, Gene expression, Humans, Hydrolysis, Immunology, Infections, Innate immunity, Intracellular Signaling Peptides and Proteins - metabolism, Intracellular Signaling Peptides and Proteins - physiology, Macrophages, Macrophages - cytology, Macrophages - microbiology, Mice, Mice, Inbred C57BL, Neutrophils, Phagocytosis, Protein Transport, Proteins, rac GTP-Binding Proteins - metabolism, Respiratory Burst - immunology, Rodents, Toll-Like Receptors - metabolism