作者: Shao-Heng He
关键词:
摘要: Historically, mast cells were known as a key cell type involved in I hypersensitivity. Until last two decades, this was recognized to be widely number of non-allergic diseases including inflammatory bowel disease (IBD). Markedly increased numbers observed the mucosa ileum and colon patients with IBD, which accompanied by great changes content such dramatically expression TNFalpha, IL-16 substance P. The evidence degranulation found wall intestine from IBD immunohistochemistry technique. highly elevated histamine tryptase levels detected strongly suggesting that is pathogenesis IBD. However, little actions histamine, tryptase, chymase carboxypeptidase Over decade, heparin has been used treat clinical practice. low molecular weight (LMWH) effective adjuvant therapy, showed good laboratory response no serious adverse effects. roles PGD2, LTC4, PAF cytokines also discussed. Recently, series experiments dispersed suggested there should at least pathways man for amplify their own activation-degranulation signals an autocrine or paracrine manner. hypothesis secretogogues induce degranulation, release then stimulate adjacent positively feedback further its host through H1 receptor. Whereas released acts similarly but activates receptor PAR-2. connections between current anti-IBD therapies potential discussed, implicating In conclusion, while remains unclear, role group demonstrated review implicates associated disease. Therefore, close attentions paid