scholarly journals Scrodentoid A Inhibits Mast Cell–Mediated Allergic Response by Blocking the Lyn–FcεRIβ Interaction

2019 ◽  
Vol 10 ◽  
Author(s):  
Fei Qian ◽  
Liuqiang Zhang ◽  
Shaodong Lu ◽  
Gaohui Mao ◽  
Fujiang Guo ◽  
...  
Keyword(s):  
2019 ◽  
Author(s):  
Joud Hajjar ◽  
Lawrence B Schwartz

The term hypersensitivity refers to diseases caused by an immune response, regardless of whether the response is against a pathogen, nonpathogen, or self and regardless of whether the response is directed by antibodies, lymphocytes, or innate pathways. The term anaphylaxis was coined in 1902 by Charles Richet, who received the Nobel Prize in 1913; this systemic allergic response is now known to be an immediate hypersensitivity reaction, initiated by allergen delivered to a host having allergen-specific IgE, thereby causing an IgE-mediated immunologic response and activating mast cells and basophils to secrete bioactive mediators. In 2005, the National Institutes of Health organized a consensus conference to develop a working definition of anaphylaxis, designed to be used by physicians at the bedside, as a serious allergic reaction that is rapid in onset, typically eliciting various combinations of cutaneous, cardiovascular, respiratory, and gastrointestinal manifestations, and may cause death.1,2 This facilitated the early treatment of such patients with epinephrine. Confusion arises over the misapplication of the term allergy or hypersensitivity to describe any untoward reaction to food, medications, or environmental exposures. Furthermore, non–IgE-mediated forms of local and systemic mast cell or basophil activation events can occur, causing signs and symptoms similar to those mediated by IgE.  This review contains 3 figures, 9 tables, and 62 references. Keywords: allergy, hypersensitivity, anaphylaxis, interleukin, chemokines, immunoglobulin E, mast cell, eosinophil


2012 ◽  
Vol 129 (5) ◽  
pp. 1357-1366.e5 ◽  
Author(s):  
Zohar Yagil ◽  
Tal Hadad Erlich ◽  
Yifat Ofir-Birin ◽  
Sagi Tshori ◽  
Gillian Kay ◽  
...  

2019 ◽  
Author(s):  
Joud Hajjar ◽  
Lawrence B Schwartz

The term hypersensitivity refers to diseases caused by an immune response, regardless of whether the response is against a pathogen, nonpathogen, or self and regardless of whether the response is directed by antibodies, lymphocytes, or innate pathways. The term anaphylaxis was coined in 1902 by Charles Richet, who received the Nobel Prize in 1913; this systemic allergic response is now known to be an immediate hypersensitivity reaction, initiated by allergen delivered to a host having allergen-specific IgE, thereby causing an IgE-mediated immunologic response and activating mast cells and basophils to secrete bioactive mediators. In 2005, the National Institutes of Health organized a consensus conference to develop a working definition of anaphylaxis, designed to be used by physicians at the bedside, as a serious allergic reaction that is rapid in onset, typically eliciting various combinations of cutaneous, cardiovascular, respiratory, and gastrointestinal manifestations, and may cause death.1,2 This facilitated the early treatment of such patients with epinephrine. Confusion arises over the misapplication of the term allergy or hypersensitivity to describe any untoward reaction to food, medications, or environmental exposures. Furthermore, non–IgE-mediated forms of local and systemic mast cell or basophil activation events can occur, causing signs and symptoms similar to those mediated by IgE.  This review contains 3 figures, 9 tables, and 62 references. Keywords: allergy, hypersensitivity, anaphylaxis, interleukin, chemokines, immunoglobulin E, mast cell, eosinophil


2016 ◽  
Vol 473 (2) ◽  
pp. 408-414 ◽  
Author(s):  
Liangchang Li ◽  
Guangyu Jin ◽  
Jingzhi Jiang ◽  
Mingyu Zheng ◽  
Yan Jin ◽  
...  

2008 ◽  
Vol 121 (5) ◽  
pp. 1225-1231 ◽  
Author(s):  
Jun Ho Lee ◽  
Jie Wan Kim ◽  
Na Young Ko ◽  
Se Hwan Mun ◽  
Erk Her ◽  
...  

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Myung-Hoon Lee ◽  
Yun Sang Lee ◽  
Haeng Jun Kim ◽  
Chang Hak Han ◽  
Sung Un Kang ◽  
...  

Abstract Non-thermal plasma (NTP) has many functional activities such as, sterilization, wound healing and anti-cancer activity. Despite of its wide spread biomedical application, the effect of NTP on immune cells and allergic response has not been well studied. In this study, we determined whether NTP suppresses mast cell activation, which is important for allergic response, and ameliorates an atopic dermatitis (AD)-like skin inflammatory disease in mice. Exposure to NTP-treated medium during mast cell activation inhibited the expression and production of IL-6, TNF-α and suppressed NF-κB activation. We also investigated whether NTP treatment ameliorates house dust mite (HDM)-induced AD-like skin inflammation in mice. NTP treatment inhibited increases in epidermal thickness and recruitment of mast cells and eosinophils, which are important cell types in AD pathogenesis. In addition, Th2 cell differentiation was induced by application of HDM and the differentiation was also inhibited in the draining lymph node of NTP-treated mice. Finally, the expression of AD-related cytokines and chemokines was also decreased in NTP-treated mice. Taken together, these results suggest that NTP might be useful in the treatment of allergic skin diseases, such as AD.


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