CAJ | 학술논문

目的：探讨心衰患者血清中β1肾上腺素受体自身抗体（β1-AA）对不同亚型T淋巴细胞增殖能力的影响。方法利用IgG亲和柱从β1-AA阳性的心衰患者血清中提纯IgG；利用流式分选技术，分选得到CD3＋CD4＋以及CD3＋CD8＋T淋巴细胞；采用CCK-8试剂盒检测β1-AA对不同亚型T淋巴细胞增殖能力的影响；使用AnnexinⅤ/PI试剂盒及乳酸脱氢酶（ LDH）水平反映细胞的损伤情况。结果β1-AA可浓度依赖性抑制活化的淋巴细胞增殖促进其损伤的发生，该效应可被β1受体阻断剂所阻断；β1-AA可诱导CD3＋CD4＋以及CD3＋CD8＋T淋巴细胞发生凋亡和坏死，并抑制其增殖。结论心衰患者血清中存在的高滴度的β1-AA可通过诱导不同亚型T 淋巴细胞发生损伤而抑制其增殖，提示，β1-AA阳性的血清除了可导致心肌损伤外还存在诱发免疫系统紊乱的危险。
목적：탐토심쇠환자혈청중β1신상선소수체자신항체（β1-AA）대불동아형T림파세포증식능력적영향。방법이용IgG친화주종β1-AA양성적심쇠환자혈청중제순IgG；이용류식분선기술，분선득도CD3＋CD4＋이급CD3＋CD8＋T림파세포；채용CCK-8시제합검측β1-AA대불동아형T림파세포증식능력적영향；사용AnnexinⅤ/PI시제합급유산탈경매（ LDH）수평반영세포적손상정황。결과β1-AA가농도의뢰성억제활화적림파세포증식촉진기손상적발생，해효응가피β1수체조단제소조단；β1-AA가유도CD3＋CD4＋이급CD3＋CD8＋T림파세포발생조망화배사，병억제기증식。결론심쇠환자혈청중존재적고적도적β1-AA가통과유도불동아형T 림파세포발생손상이억제기증식，제시，β1-AA양성적혈청제료가도치심기손상외환존재유발면역계통문란적위험。
Objective To investigate the effects of β1-adrenergic receptor autoantibodies (β1-AA) on the proliferation of different subtypes of T lymphocytes in patients with heart failure .Methods β1-AA-positive IgG antibodies isolated from patients with heart failure were purified by using affinity chromatog -raphy.CD3 +CD4 +T and CD3 +CD8 +T lymphocytes were sorted by flow cytometry analysis .The prolifera-tion of different subtypes of T lymphocytes was tested by using CCK-8 kit.Tests for lactate dehydrogenase ( LDH) level and cell apoptosis were performed to evaluate T lymphocytes damage .Results The prolifera-tion of activated lymphocytes was inhibited by β1-AA isolated from the serum of patients with heart failure in a concentration dependent manner , but it could be blocked by β1 receptor blocker .The damage of lympho-cytes induced by β1-AA was increased.Moreover, β1-AA promoted the necrosis and apoptosis of CD 3 +CD4 +T and CD3 +CD8 +T lymphocytes and thus inhibited the proliferation of them .Conclusion β1-AA isolated from the serum of patients with heart failure inhibited the proliferation of CD 3 +CD4 +T and CD3 +CD8 +T lymphocytes through increasing the necrosis and apoptosis of them .This study suggests that β1-AA might induce immune disorders in addition to causing pathological changes in heart tissues .