Influence of immune complexes containing HBsAg and HBeAg on IL-2 dependent human lymphocyte proliferation.

Allergie und Immunologie Pub Date : 1990-01-01
J Stachowski, J Michalkiewicz, H Gregorek, K Madalinski, J Maciejewski
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Abstract

Studies were undertaken to evaluate the effect of hepatitis B virus (HBV) immune complexes (HBV-IC) on IL-2 dependent human lymphocyte proliferation. The following parameters were studied: 1) Effect of HBV-IC (HBsAg-IgG or HBeAg-IgG) on PHA-mediated lymphocyte proliferation; 2) Influence of HBV-IC on the ability of PHA-stimulated peripheral blood lymphocytes (PBL) for IL-2 production and IL-2 receptor expression. HBV-IC induced a dose dependent and antigenic dependent suppression of PHA stimulated lymphocytes. The suppressor effect exerted by HBsAg-IgG was irreversible. In contrast, the suppression mediated by HBeAg-IgG was reversible: lymphocytes preincubated with this preparation washed and activated with PHA responded well to mitogen. The presence of HBV-IC in the cultures of PHA-activated PBL decreased their ability to produce IL-2: HBeAg-IgG exerted a stronger suppressor effect. This effect was partially reversible: removal of HBV-IC from the culture by washing and subsequent stimulation of PBL with PHA increased the capacity of lymphocytes to produce IL-2. This was particularly evident with HBeAg-IgG. Decreased activity of IL-2 observed in the cultures, was also partially dependent on the ability of HBV-IC to bind IL-2 present in the culture medium. Experiments performed using ultracentrifugation indicated that HBV-IC, especially HBsAg-IgG, may bind to IL-2 and inactivate it. HBV-IC had also an effect on IL-2 receptor expression: 1) their presence in the cultures of PHA-stimulated PBL decreased the number of Tac positive cells; 2) the response of HTCL to exogenous IL-2 was decreased by HBV-IC present in the culture medium. This was especially observed in the case of HBsAg-IgG. We suggest that the observed inhibition of PHA-induced lymphocyte proliferation exerted by immune complexes containing HBsAg-IgG or HBeAg-IgG may be caused mainly by their influence on IL-2 dependent mechanism of lymphoproliferation.

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含HBsAg和HBeAg的免疫复合物对IL-2依赖性人淋巴细胞增殖的影响。
研究评估了乙型肝炎病毒(HBV)免疫复合物(HBV- ic)对IL-2依赖性人淋巴细胞增殖的影响。研究以下参数:1)HBV-IC (HBsAg-IgG或HBeAg-IgG)对pha介导的淋巴细胞增殖的影响;2) HBV-IC对pha刺激的外周血淋巴细胞(PBL)产生IL-2和IL-2受体表达能力的影响。HBV-IC诱导PHA刺激淋巴细胞的剂量依赖性和抗原依赖性抑制。HBsAg-IgG的抑制作用是不可逆的。相比之下,HBeAg-IgG介导的抑制是可逆的:用这种制剂预先孵育的淋巴细胞经PHA洗涤和活化后,对有丝分裂原反应良好。在pha激活的PBL中,HBV-IC的存在降低了它们产生IL-2的能力,而HBeAg-IgG具有更强的抑制作用。这种效果是部分可逆的:通过清洗和随后用PHA刺激PBL,从培养物中去除HBV-IC,增加淋巴细胞产生IL-2的能力。这在HBeAg-IgG中尤为明显。在培养物中观察到IL-2活性降低,也部分依赖于HBV-IC结合培养基中存在的IL-2的能力。超离心实验表明,HBV-IC,特别是HBsAg-IgG可能与IL-2结合并使其失活。HBV-IC对IL-2受体的表达也有影响:1)它们在pha刺激的PBL培养物中的存在减少了Tac阳性细胞的数量;2)培养基中存在HBV-IC降低了HTCL对外源IL-2的反应。这在HBsAg-IgG的情况下尤其明显。我们认为,含有HBsAg-IgG或HBeAg-IgG的免疫复合物对pha诱导的淋巴细胞增殖的抑制作用可能主要是由于它们影响了依赖IL-2的淋巴细胞增殖机制。
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