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The counter-regulation of atherogenesis: a role for interleukin-33 Kunes P; Holubcova Z; Kolackova M; Krejsek JActa Medica (Hradec Kralove) 2010[]; 53 (3): 125-9The recently recognized cytokine interleukin-33 and its receptor ST2 play a favorable role during atherogenesis by inducing a Th1 --> Th2 shift of the immune response. IL-33 also protects the failing human heart from harmful biomechanical forces which lead to cardiomyocyte hypertrophy and exaggerated interstitial fibrosis. IL-33 inevitably displays side effects common to other Th2 cytokines, the most grave of which is a predisposition to allergic reactions. IL-33 is a nuclear transcription factor of endothelial cells. As such, it is abundant in nonproliferating vessels. Its down-regulation is required for angiogenesis, which may be profitable in wound healing or deleterious in tumor growth.|Animals[MESH]|Atherosclerosis/immunology/*physiopathology[MESH]|Down-Regulation[MESH]|Humans[MESH]|Interleukin-1 Receptor-Like 1 Protein[MESH]|Interleukin-33[MESH]|Interleukins/immunology/*physiology[MESH]|Receptors, Cell Surface/physiology[MESH]|Th1 Cells/immunology/physiology[MESH]|Th2 Cells/immunology/physiology[MESH] |
