Histamine synthesis by mouse T lymphocytes through induced histidine decarboxylase.
Histamine synthesis by mouse T lymphocytes through induced histidine decarboxylase.
复制标题
小鼠 T 淋巴细胞通过诱导组氨酸脱羧酶合成组胺。
作者：
R. Aoi;I. Nakashima;Y. Kitamura;H. Asai;K. Nakano
培养C57BL/6小鼠和肥大细胞缺陷W/WV小鼠的脾细胞，其组氨酸脱羧酶(HDC)活性随细胞和培养液中组胺浓度的增加而升高。刀豆蛋白A(ConA)或大肠杆菌脂多糖(LPS)的加入促进了这种增加。黏附细胞的去除降低了对照HDC的活性和对有丝分裂原的反应。纯化的T淋巴细胞对刀豆蛋白A有反应，但对脂多糖无反应。刀豆蛋白A和脂多糖对B淋巴细胞均无影响。用抗Thy-1.2抗体和补体处理T细胞，可完全阻断HDC的诱导。用内毒素激活的腹膜贴壁细胞加入条件培养液，刺激T细胞依赖ConA合成组胺。加入重组白介素1(rIL-1)或多聚甲醛固定的腹膜贴壁细胞可显著增强T细胞对ConA依赖的HDC的诱导。这些结果表明，组胺是由T淋巴细胞通过HDC合成的，巨噬细胞释放的一种可溶性因子(S)促进了这一反应。
When spleen cells of C57BL/6 mice or mast cell-deficient W/Wv mice were cultured, their histidine decarboxylase (HDC) activity increased with increases in the histamine concentration in the cells and the medium. Addition of concanavalin A (Con A) or Escherichia coli lipopolysaccharide (LPS) enhanced the increase. The removal of adherent cells reduced both the control HDC activity and the response to the mitogens. Purified T lymphocytes responded to Con A but not to LPS. Neither Con A nor LPS had any effect on B lymphocytes. Treatment of T cells with anti-Thy-1.2 and complement completely abrogated the induction of HDC. Histamine synthesis dependent on Con A by T cells was stimulated by the addition of conditioned medium from peritoneal adherent cells activated with LPS. The addition of recombinant interleukin-1 (rIL-1) or peritoneal adherent cells fixed with paraformaldehyde significantly enhanced HDC induction dependent on Con A in T cells. These results suggest that histamine is synthesized by T lymphocytes through HDC and that the reaction was enhanced by a soluble factor(s) released from macrophages.