Immunity . . . Significant progress has been made by Wang Honglin of Shanghai Jiaotong University, among others, which revealed the mechanism of abnormally aggravated psoriasis in metabolic processes.

Inature psoriasis is a chronic inflammatory disease, its etiology is multifactorial.the effect of cell metabolism on psoriasis is not clear.on June 17, 2020, Wang Honglin of Shanghai Jiaotong University and Florent ginhoux jointly published an online publication entitled "excessive polyamine generation in keratinocytes promoters self RNA sensing by democratic cells in" immunity This study found that interleukin-17 (IL-17) down regulated protein phosphatase 6 (pp6) in psoriatic keratinocytes, resulting in phosphorylation and activation of transcription factor C / EBP - β, and subsequent arginase-1 production.mice lacking pp6 in keratinocytes are prone to psoriasis like skin inflammation.accumulation of arginase-1 in keratinocytes with pp6 deficiency drives urea cycle to produce polyamines.polyamines can protect the self RNA released by psoriatic keratinocytes from degradation and promote the endocytosis of their own RNA by myeloid dendritic cells, thus promoting toll like receptor 7 (TLR7) - dependent RNA induction and IL-6 production.in the animal model of psoriasis, the non primate arginine inhibitor was improved.this study showed that the urea cycle overreaction and excessive polyamine production in keratinocytes of psoriasis can promote self RNA induction, and the imbalance of pp6 in keratinocytes is a key event, which can amplify the inflammatory circuit of psoriasis.psoriasis is characterized by an abnormal interaction between hyperplastic keratinocytes and self reactive immune cells.although psoriasis has long been regarded as a metabolic disease and is believed to be facilitated by the intrinsic metabolic flux of keratinocytes, the metabolic adaptive arrangement and potential mechanism of psoriasis remain unclear.abnormal metabolism of amino acids and lipids is found in psoriasis patients - saturated fatty acids in the diet can aggravate skin inflammation.at the same time, inhibition of glucose transport in keratinocytes seems to be another treatment for psoriasis.however, the presence of tissue-specific metabolism and its functional importance in the context of inflammation may be unknown.another aspect of the auto inflammatory cycle in the pathogenesis of psoriasis is innate immune activation, which triggers subsequent adaptive immune responses to its own components.LL-37, adamtsl5, new lipids and hnRNPA1 are possible autoantigens of psoriasis, and LL-37 and hnRNPA1 have RNA binding properties.in view of the importance of self RNA sensing in the development of inflammatory diseases such as psoriasis and lupus, how antigen presenting cells process these RNA binding proteins and make them become antigens needs to solve the problem of self reactive T cell recognition.the article pattern (image from immunity) previously reported that microrna-31 targeted protein phosphatase 6 (pp6) is a negative cell cycle regulator in psoriatic keratinocytes. pp6 is essential for skin dynamic balance. considering the versatility of serine / threonine phosphatase, the aim of this study was to determine the specific function of pp6 in keratinocytes. this study found that interleukin-17 (IL-17) downregulated protein phosphatase 6 (pp6) in psoriatic keratinocytes, resulting in phosphorylation and activation of transcription factor C / EBP - β and subsequent arginase-1 production. mice lacking pp6 in keratinocytes are prone to psoriasis like skin inflammation. accumulation of arginase-1 in keratinocytes with pp6 deficiency drives urea cycle to produce polyamines. polyamines can protect the self RNA released by psoriatic keratinocytes from degradation and promote the endocytosis of their own RNA by myeloid dendritic cells, thus promoting toll like receptor 7 (TLR7) - dependent RNA induction and IL-6 production. arginase inhibitors improved skin inflammation in rat and non-human primate animal models of psoriasis. this study showed that the urea cycle overreaction and excessive polyamine production in keratinocytes of psoriasis can promote self RNA induction, and the imbalance of pp6 in keratinocytes is a key event, which can amplify the inflammatory circuit of psoriasis. reference message: ා% 20