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Interleukin (IL)-36, a member of the IL-1 family, plays an important role in mediating inflammatory diseases .IL-36 subfamily consists of IL-36α, IL-36β, IL-36γand IL-36 receptor antagonists (IL-36Ra).IL-36 receptor (IL-36R) and IL-1 receptor accessory protein (IL-1RAcP) are involved in the IL-36-mediated signal transduction .In human, mutations in the gene encoding IL-36Ra will lead to IL-36R signaling disorders , mainly manifested as diffuse pustular psoriasis .It suggests that IL-36 plays an important role in psoriasis.Recently, it has also been found that IL-36 is related to inflammation in other organs . These emerging roles of IL-36 provide new thoughts for the treatment of human inflammatory diseases .
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Type II innate lymphoid cells ( ILC2s) are widely distributed in the blood , intestines, trachea, lung, spleen, liver, animal fat and skin, and involved in the innate immune responses .ILC2s have attracted much atten-tion for its important roles in the conversion of white adipose to beige adipose .Studies have shown that ILC2s are essential for the proliferation and differentiation of adipocyte precursor cells , and they also play a vital role in anti-parasitic infection and allergic inflammation .This review discusses the discovery , differentiation , development , distribution and function of ILC2s, and their relationships with the browning of white adipose tissue for providing valuable references on understanding the pathogenesis , prevention and treatment of obesity and fat metabolism disorders .
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Nuclear factor(NF)-κB is widely expressed in various types of tissue cells. Abnormal activation of NF-κB signaling pathway can lead to the initiation and progression of asthma,chronic ob?structive pulmonary disease(COPD)and other lung inflammatory diseases,but inhibition of its activity can effectively alleviate the occurrence and development of these diseases. In this paper ,we review biological characteristics of NF-κB,role of NF-κB signaling in asthma,COPD and other inflammatory lung diseases,and potential application of NF-κB inhibitors in clinical treatment of these inflammatory lung diseases. It will provide a valuable reference for further study on pathogenesis,prevention,and control of lung inflammatory diseases.
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Objective:To predict the secondary structure and B-cell epitope of human IL-37.Methods:Based on IL-37b ami-no acid sequence, the secondary structure was predicted by SOPMA; hydrophilicity, flexibility, accessibility index were predicted by software of ProScale, Bcepred, respectively.Combined the results according to these methods , the B cell epitopes of IL-37b were pre-dicted.Results: The second structure of IL-37b contained extended strand (31.65%), random coil (52.75%), alpha helix (8.26%), beta turn (7.34%) and the most possible epitopes of IL-37b were located in or adjacent to amino acid 21-27, 34-75, 175-192 , 213-215 .Conclusion:These results will be helpful for the estimate of the epitopes and provide a theory basis for developing mon -oclonal antibodies against human IL-37.
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There is a rapid increase in medical information in the internet,so it is necessary for medical workers to know how to search and get the useful medical information. The medical information can be obtained by some search engines and internet address.
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Transforming growth factor-?(TGF-?)was reported to be increased in asthma in some studies. Accumulation of TGF-? in airway promotes smooth muscle cell mitogenesis and hyperplasia, and induces fibroblast and myofibroblast and smooth muscle proliferation as well as increase in protein synthesis in connective tissue(such as collagen deposition on the reticular basement membrane). The autocrine induction of collagen expression by smooth muscle may contribute to the thickening of the reticular basement membrane, irreversible fibrosis and remodeling seen in the airways in some asthmatics. TGF-? is considered to be a major fibrogenic cytokine. It can increase smooth muscle mass and lead to severe bronchial obstruction in an asthma attack.