EFFECTS OF BRUCELLA ABORTUS AND LPS-BA ON LYMPHOKINE SECRETION

我们感兴趣的是BA作为人类发展的载体 疫苗，因为它的行为作为一个T-非依赖性1型抗原， 刺激人B细胞。 也就是说，它能够诱导人类B 细胞反应（i）在T细胞相对缺乏的情况下，（ii）新生儿 人B细胞和（iii）从患有 Wiskott-Aldrich综合征（X连锁免疫缺陷）。 这些属性 表明BA可能特别适合作为HIV-1携带者 诱导HIV-1感染者应答的衍生蛋白或肽 个体（CD 4 + T细胞功能受损）和新生儿， HIV-1感染的母亲。 最近的证据表明，BA 部分依赖于T细胞因子，特别是IFNg。 在小鼠中， 诱导IFNg的能力可能与BA 以高滴度为特征的特定IgG亚类模式 IgG 2a。 这在病毒感染的背景下可能很重要，因为 IgG 2a对补体和Fc受体具有高亲和力。 主要 本课题的目的是研究BA对人T细胞的影响， 细胞，特别是在IFNg释放方面。 我很感兴趣的是， 确定BA是否可以触发CD 8 + T细胞亚群，因为这些 细胞保留在HIV-1感染的个体中。 刺激这些 后一种细胞可以诱导淋巴因子，从而绕过对淋巴细胞的需要。 CD 4+和CD 8+人T细胞能够应答BA， 分泌IFNg 人T细胞向BA释放IFNg可能是 在IL 2存在下协同增加。 这种协同作用是 这可能与BA能增加IL-2的表达有关 人T细胞表面的受体。我们用流动来证明 细胞仪

We are interested in BA as a carrier in the development of human vaccines because it behaves as a T-independent type 1 antigen in stimulating human B cells. That is, it is capable of inducing human B cell responses (i) in the relative absence of T cells, (ii) in neonatal human B cells and (iii) in B cells obtained from patients with the Wiskott-Aldrich syndrome (X-linked immunodeficiency). These properties suggest that BA may be particularly well suited as a carrier for HIV-1 derived proteins or peptides in eliciting responses from HIV-1 infected individuals (with compromised CD4+ T cell function) and in neonates who have HIV-1 infected mothers. Recent evidence suggests that BA is partially dependent on T cell factors, in particular IFNg. In mice this ability to induce IFNg is probably related to the observation that BA elicits a certain IgG subclass pattern characterized by high titer IgG2a. This may be important in the context of viral infections because IgG2a has high affinity for complement and Fc receptors. The main purpose of this project was to investigate the effect of BA on human T cells, especially with respect to IFNg release. It was of interest to determine whether BA could trigger the CD8+ T cell subset because these cells are retained in HIV-1 infected individuals. Stimulation of these latter cells may induce lymphokines and thus bypass the requirement for CD4+ and CD8+ human T cells were capable of responding to BA and secreting IFNg. The IFNg release by human T cells to BA could be synergistically increased in the presence of IL2. This synergism was probably due to the fact that BA could increase the expression of IL-2 receptor on the surface of human T cells. which we demonstrated by flow cytometry.