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首页> 外文期刊>Hepatology: Official Journal of the American Association for the Study of Liver Diseases >Mechanism of T cell tolerance induction by murine hepatic Kupffer cells.
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Mechanism of T cell tolerance induction by murine hepatic Kupffer cells.

机译：鼠肝库普弗细胞诱导T细胞耐受的机制。

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The liver is known to favor the induction of immunological tolerance rather than immunity. Although Kupffer cells (KC) have been indicated to play a role in liver tolerance to allografts and soluble antigens, the mechanisms involved remain unclear. We hypothesized that KCs could promote immune tolerance by acting as incompetent antigen-presenting cells (APC), as well as actively suppressing T cell activation induced by other potent APCs. The expression of antigen presentation-related molecules by KCs was phenotyped by flow cytometry. The abilities of KCs to act as APCs and to suppress T cell activation induced by splenic dendritic cells (DC) were examined by in vitro proliferation assays using CD4(+) OVA-TCR (ovalbumin T cell receptor) transgenic T cells. We found that, compared with DCs, KCs expressed significantly lower levels of major histocompatibility complex (MHC) II, B7-1, B7-2, and CD40. This result is consistent with our observation that KCs were not as potent as DCs in eliciting OVA-specific T cell proliferation. However, KCs isolated from polyinosinic:polycytidylic acid-treated mice expressed significantly higher levels of MHC II and costimulatory molecules than did naive KCs and could stimulate stronger T cell responses. More importantly, we found that KCs could inhibit DC-induced OVA-specific T cell activation. Further investigation of the underlying mechanism revealed that prostaglandins produced by KCs played an important role. The results ruled out the possible involvement of interleukin-10, nitric oxide, 2,3-dioxygenase, and transforming growth factor beta in KC-mediated T cell suppression. Conclusion: Our data indicate that KCs are a tolerogenic APC population within the liver. These findings suggest that KCs may play a critical role in regulating immune reactions within the liver and contributing to liver-mediated systemic immune tolerance. (HEPATOLOGY 2008.).
机译：已知肝脏有利于诱导免疫耐受而不是免疫。尽管已经表明库普弗细胞（KC）在肝脏对同种异体移植物和可溶性抗原的耐受性中起作用，但所涉及的机制仍不清楚。我们假设KCs可以通过充当无能的抗原呈递细胞（APC）来促进免疫耐受，并积极抑制其他有效APC诱导的T细胞活化。通过流式细胞术对抗原呈递相关分子在KCs中的表达进行表型分析。使用CD4（+）OVA-TCR（卵清蛋白T细胞受体）转基因T细胞进行体外增殖测定，检验了KC充当APC并抑制脾树突状细胞（DC）诱导的T细胞活化的能力。我们发现，与DC相比，KC表达的主要组织相容性复合物（MHC）II，B7-1，B7-2和CD40的水平明显降低。这个结果与我们的观察结果一致，即KC在诱发OVA特异性T细胞增殖方面不如DC有效。但是，从幼肌细胞：聚胞苷酸治疗的小鼠中分离出的KCs比幼稚KCs的MHC II和共刺激分子水平高得多，并且可以刺激更强的T细胞反应。更重要的是，我们发现KCs可以抑制DC诱导的OVA特异性T细胞活化。对潜在机制的进一步研究表明，KC产生的前列腺素起着重要作用。结果排除了白介素10，一氧化氮，2，3-二加氧酶和转化生长因子β可能参与KC介导的T细胞抑制。结论：我们的数据表明，KCs是肝脏内的一种致耐受性APC种群。这些发现表明，KCs可能在调节肝脏内的免疫反应和促进肝脏介导的全身免疫耐受中起关键作用。 （HEPATOLOGY 2008.）。

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