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Fig. 2 | Cell & Bioscience

Fig. 2

From: Deciphering the role of interleukin-22 in metabolic alterations

Fig. 2

Role of endogenous IL-22 in the development of adiposity and metabolic alterations in mice and men. Adiposity can be induced by high caloric diet in mice and humans. Respective mouse models are based on massively forced fat intake of animals kept under pathogen-free conditions and usually involves very young mice (they are typically analyzed at an age of 20 % of their maximum age). Using such models, IL-22-deficient mice do not show a specific phenotype, although the activation of IL-22R1 by endogenous ligands seems to moderately limit the development of adiposity and metabolic alterations. In contrast to these mouse models, the development of adiposity and metabolic alterations in humans usually takes long time periods and leads to death within the second half of life. Importantly, banal infections or injury that occur over the extended time period might amplify the generation of IL-22-producing cells. We postulate that this endogenous IL-22 is a new counter-mechanism of the immune system to limit the development of adiposity and metabolic alterations

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