Regulation of the innate immune response by threonine-phosphatase of Eyes absent
作者： Yasutaka Okabe , Teruyuki Sano , Shigekazu Nagata
DOI: 10.1038/NATURE08138
关键词:
摘要: Innate immunity is stimulated not only by viral or bacterial components, but also non-microbial danger signals (damage-associated molecular patterns). One of the damage-associated patterns chromosomal DNA that escapes degradation. In programmed cell death and erythropoiesis, from dead cells nuclei expelled erythroblasts digested DNase II in macrophages after they are engulfed. II(-/-) (also known as Dnase2a(-/-)) mice suffer severe anaemia chronic arthritis due to interferon-beta (IFN-beta) tumour necrosis factor-alpha (TNF-alpha) produced carrying undigested a Toll-like receptor (TLR)-independent mechanism. Here we show Eyes absent 4 (EYA4), originally identified co-transcription factor, stimulates expression IFN-beta CXCL10 response apoptotic cells. EYA4 enhanced innate immune against viruses (Newcastle disease virus vesicular stomatitis virus), could associate with signalling molecules (IPS-1 MAVS), STING (TMEM173) NLRX1). Three groups have previously shown EYA has phosphatase activity. We found mouse family members act for both phosphotyrosine phosphothreonine. The haloacid dehalogenase domain at carboxy terminus contained tyrosine-phosphatase, amino-terminal half carried threonine-phosphatase. Mutations threonine-phosphatase, abolished ability enhance response, suggesting regulates modulating phosphorylation state signal transducers intracellular pathogens.
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