组胺
组氨酸脱羧酶
白细胞介素33
组胺H4受体
脱颗粒
肥大细胞
造血
免疫学
白细胞介素5
白细胞介素3
细胞因子
干细胞因子
生物
化学
白细胞介素
细胞生物学
受体
医学
组胺H2受体
抗原提呈细胞
内科学
T细胞
内分泌学
免疫系统
干细胞
组氨酸
生物化学
氨基酸
敌手
作者
Kanan Bando,Yukinori Tanaka,Saka Winias,Shunji Sugawara,Itaru Mizoguchi,Yasuo Endo
标识
DOI:10.1007/s00011-023-01699-y
摘要
IL-33 is present in endothelial, epithelial, and fibroblast-like cells and released upon cell injury. IL-33 reportedly induces mast-cell degranulation and is involved in various diseases, including allergic diseases. So, IL-33-related diseases seem to overlap with histamine-related diseases. In addition to the release from mast cells, histamine is newly formed by the induction of histidine decarboxylase (HDC). Some inflammatory and/or hematopoietic cytokines (IL-1, IL-3, etc.) are known to induce HDC, and the histamine produced by HDC induction is released without storage. We examined the involvement of HDC and histamine in the effects of IL-33.A single intraperitoneal injection of IL-33 into mice induced HDC directly and/or via other cytokines (including IL-5) within a few hours in various tissues, particularly strongly in hematopoietic organs. The major cells exhibiting HDC-induction were mast cells and c-kit+ cells in the bone marrow. HDC was also induced in non-mast cells in non-hematopoietic organs. HDC, histamine, and histamine H4 receptors (H4Rs) contributed to the suppression of IL-33-induced eosinophilia.IL-33 directly and indirectly (via IL-5) induces HDC in various cells, particularly potently in c-kit+ cells and mature mast cells, and the newly formed histamine contributes to the negative regulation of IL-33-induced eosinophilia via H4Rs.
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