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自身免疫性疾病小鼠中淋巴细胞抑素活性的丧失。

Loss of lymphocyte chalone activity in mice with autoimmune disease.

作者信息

Attallah A M, Steinberg A D, Ahmed A, Sell K W

出版信息

Int Arch Allergy Appl Immunol. 1979;59(2):186-91. doi: 10.1159/000232257.

Abstract

Lymphocyte chalone from the spleens of old BALB/c, young BALB/c and young NZB mice caused significant suppression of the proliferative response of BALB/c and NZB spleen cells to T and B mitogens, whereas lymphocyte chalone from old NZB spleen did not suppress. Lymphocyte chalone from young and old NZB mice was tested using different ages of NZB/NZW responding spleen cells; at all ages concanavalin A- and lipopolysaccharide-induced proliferation was suppressed less by the chalone from old NZB mice than from that of young NZB mice. The responding NZB/NZW cells were suppressed equivalently at all ages studied. The basis for the loss of lymphocyte chalone activity in old NZB mice remains unknown; however, it appears likely that this event has a role in the disturbance of the negative feedback control system which contributes to NZB autoimmune disease.

摘要

来自老年BALB/c、年轻BALB/c和年轻NZB小鼠脾脏的淋巴细胞抑素可显著抑制BALB/c和NZB脾细胞对T和B有丝分裂原的增殖反应,而来自老年NZB脾脏的淋巴细胞抑素则无抑制作用。使用不同年龄的NZB/NZW反应性脾细胞对年轻和老年NZB小鼠的淋巴细胞抑素进行了测试;在所有年龄段,与年轻NZB小鼠相比,老年NZB小鼠的抑素对刀豆球蛋白A和脂多糖诱导的增殖的抑制作用较小。在所有研究的年龄段,反应性NZB/NZW细胞受到的抑制程度相同。老年NZB小鼠淋巴细胞抑素活性丧失的原因尚不清楚;然而,这一事件似乎可能在导致NZB自身免疫性疾病的负反馈控制系统紊乱中起作用。

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