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CLEC7A — IL22

Text-mined interactions from Literome

Mezger et al., J Infect Dis 2008 (Aspergillosis) : Silencing of dectin-1 resulted in reduced expression of proinflammatory cytokines ( tumor necrosis factor-alpha and interleukin-12 ), which was also reduced by anti-Dectin-1 antibody treatment prior to exposure to A. fumigatus, zymosan, or Candida albicans
Gessner et al., Infect Immun 2012 (Pulmonary Aspergillosis) : Dectin-1 dependent interleukin-22 contributes to early innate lung defense against Aspergillus fumigatus ... As IL-23 is also thought to control the production of IL-22, we examined the role of Dectin-1 in IL-22 production, as well as the role of IL-22 in innate host defense against A. fumigatus ... Culturing cells from enzymatic lung digests ex vivo further demonstrated Dectin-1 dependent IL-22 production ... Collectively, our results indicate that early innate lung defense against A. fumigatus is mediated by Dectin-1 dependent IL-22 production
Lilly et al., J Immunol 2012 (Chronic Disease...) : Assessment of Th responses demonstrated that purified lung CD4 ( + ) T cells produced IL-4, IL-13, IFN-?, and IL-17A, but not IL-22 , in a Dectin-1 dependent manner ... In contrast, we observed robust, Dectin-1 dependent IL-22 production by unfractionated lung digest cells ... Intriguingly, the absence of IL-22 alone mimicked the attenuated proallergic and proinflammatory responses observed in the absence of Dectin-1, suggesting that Dectin-1 mediated IL-22 production potentiated responses that led to decrements in lung function