首页> 美国卫生研究院文献>Clinical and Experimental Immunology >Immunoregulation of the in vitro anti-HBs antibody synthesis in chronic HBsAg carriers and in recently boosted anti-hepatitis B vaccine recipients.
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Immunoregulation of the in vitro anti-HBs antibody synthesis in chronic HBsAg carriers and in recently boosted anti-hepatitis B vaccine recipients.

机译:在慢性HBsAg携带者中以及最近在增加抗乙肝疫苗接种者中的体外抗HBs抗体合成的免疫调节。

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摘要

We report a study on immunoregulation of in vitro antibody to hepatitis B surface antigen (anti-HBs) synthesis induced by pokeweed mitogen (PWM) from peripheral blood mononuclear cells (PBMC) in chronic hepatitis B surface antigen (HBsAg) carriers and in 'high responders', (anti-HBs RIA ratio greater than or equal to 20 in serum), recently boosted with anti-hepatitis B vaccine. Anti-HBs was detected in 11 days PBMC supernatants (SN) from 24 out of 36 'high responders', but in none from 31 chronic HBsAg carriers, despite detectable amounts of polyclonal IgG and antibody to hepatitis B core antigen (anti-HBc) were produced. The lack of anti-HBs production by chronic HBsAg carriers did not seem to be determined by suppressor influences because T lymphocytes from the majority of chronic HBsAg carriers, co-cultured with 'high responders' PBMC did not suppress anti-HBs production. Co-cultures between HBsAg carriers T4 positive (helper/inducer) cells and allogenic 'high responder' non-T cells produced anti-HBs antibody, indicating that HBsAg carrier T cells are not deficient in this allogenic helper function under PWM stimulation. Allogenic cocultures between HBsAg carrier non-T cells and 'high responder' T4 positive cells failed in anti-HBs production: a specific B lymphocyte defect might be involved in the lacking anti-HBs synthesis in chronic HBV patients. Antigen-induced specific anti-HBs synthesis experiments indicate that B cells themselves seem to be the target for HBsAg-induced suppression of anti-HBs antibody response.
机译:我们报告了对慢性乙型肝炎表面抗原(HBsAg)携带者和外周血单个核细胞(PBMC)中的商陆有丝分裂原(PWM)诱导的商陆乙肝表面抗原(PWM)合成的体外抗体免疫调节的研究最近,抗乙型肝炎疫苗提高了应答者的抵抗力(血清中抗HBs RIA比率大于或等于20)。在36天的“高应答者”中有24天的PBMC上清液(SN)中有11天检测到抗HBs,但在31例慢性HBsAg携带者中均未检测到,尽管可检测到多克隆IgG和抗乙型肝炎核心抗原的抗体(anti-HBc)被生产了。慢性HBsAg携带者缺乏抗HBs的产生似乎不是由抑制因素决定的,因为大多数慢性HBsAg携带者的T淋巴细胞与“高反应者” PBMC共培养不能抑制抗HBs的产生。 HBsAg载体T4阳性(辅助/诱导)细胞与同种异体“高反应性”非T细胞共培养产生抗HBs抗体,表明HBsAg载体T细胞在PWM刺激下并不缺乏这种同种异体辅助功能。 HBsAg携带者非T细胞与“高反应性” T4阳性细胞之间的同种异体培养无法产生抗HBs:在慢性HBV患者中,特定的B淋巴细胞缺陷可能与缺乏抗HBs合成有关。抗原诱导的特异性抗HBs合成实验表明,B细胞本身似乎是HBsAg诱导的抗HBs抗体反应抑制的靶标。

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