Bulletin du Groupement international pour la recherche scientifique en stomatologie & odontologie最新文献

The role of infectious agents in autoimmune diseases genesis is still a matter of debate. Several observations have suggested that autoimmune diseases may be initiated or worsened by infections (review by Kivity et al., 2009). However, there is no clear understanding of the underlying mechanisms. In particular, autoantibody production during infections could be the result of the non specific activation of “natural” autoreactive B cells that produce only low-affinity antibodies (Lacroix-Desmazes et al., 1998). A relevant hypothesis making the link between infections and autoimmune diseases could be the progressive genesis of more affine autoreactive B cells that could be involved in different pathogenic conditions. The major purpose of our work is therefore to study the breakdown of B cell tolerance and the ability for autoreactive B cells,especially low reactive B cells, to engage in an affinity maturation process during infections.We have created a new autoreactive B cell model allowing a relevant study of affinity maturation process. In this intermediate affinity SWHEL X HEL2x autoreactive model, knock-in B cells (Taki etal., 1993) express a B cell receptor highly specific for Hen-Egg Lysozyme (HEL) that recognizes HEL2x mutated auto-antigen with intermediate affinity (Phan et al., 2003; SWHEL model).Phenotypic analysis revealed that these autoreactive B cells are in a state of partial tolerance compared to the high affinity model (Phan et al., 2003; SWHEL X ML5 model) characterized by a strong anergy of HEL positive B cells.Experimental infections were performed with Borrelia burgdorferi, a Gram-negative spirochete,leading to sustained lymph nodes polyclonal B cell activation and hypergammaglobulinemia (Soulas et al., 2005). In SWHEL X HEL2x infected mice, in the presence of their auto-antigen,intermediate affinity autoreactive B cells are able to proliferate, to be activated, to enter into lymph nodes germinal centers and to produce IgM and IgG autoantibodies, although in low amounts.Moreover, IgG auto-antibodies in infected mice appear somatically mutated in the auto-antigen recognizing area. These data are consistent with a partial tolerance breakdown and the next experimental step will consist in checking the long-term survival of such activated autoreactive B cells and the impact of the observed mutations

感染因子在自身免疫性疾病发生中的作用仍然是一个有争议的问题。一些观察结果表明，自身免疫性疾病可能由感染引发或恶化(Kivity等人，2009年的综述)。然而，对潜在的机制还没有明确的认识。特别是，感染期间自身抗体的产生可能是“天然”自身反应性B细胞非特异性激活的结果，这些B细胞只产生低亲和力抗体(Lacroix-Desmazes等，1998)。在感染和自身免疫性疾病之间建立联系的一个相关假设可能是更多的仿射性自身反应性B细胞的渐进发生，这些细胞可能参与不同的致病条件。因此，我们工作的主要目的是研究B细胞耐受性的破坏以及自身反应性B细胞，特别是低反应性B细胞在感染过程中参与亲和力成熟过程的能力。我们已经创建了一个新的自反应性B细胞模型，允许亲和成熟过程的相关研究。在这个中等亲和力的SWHEL X HEL2x自反应模型中，敲入B细胞(Taki etal.)。(Phan et al.， 2003)表达一种高度特异性的B细胞受体，用于识别HEL2x突变的自身抗原，具有中等亲和力(Phan et al.， 2003);SWHEL模型)。表型分析显示，与高亲和力模型相比，这些自身反应性B细胞处于部分耐受状态(Phan等，2003;SWHEL X ML5模型)以HEL阳性B细胞能量强为特征。实验用革兰氏阴性螺旋体伯氏疏螺旋体进行感染，导致持续的淋巴结多克隆B细胞活化和高γ球蛋白血症(Soulas等，2005年)。在感染SWHEL X HEL2x的小鼠中，在自身抗原存在的情况下，中等亲和力的自身反应性B细胞能够增殖，被激活，进入淋巴结生发中心并产生IgM和IgG自身抗体，尽管数量很低。此外，感染小鼠的IgG自身抗体在自身抗原识别区出现体细胞突变。这些数据与部分耐受性破坏一致，下一个实验步骤将包括检查这些活化的自身反应性B细胞的长期存活和观察到的突变的影响

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Detection and characterization of circulating endothelial cells in multiple myeloma versus monoclonal gammapathy of indeterminated signifiance. 循环内皮细胞在多发性骨髓瘤中的检测和表征与单克隆γ病的不确定意义。

Bulletin du Groupement international pour la recherche scientifique en stomatologie & odontologie

Pub Date : 2011-11-22

C Cabasse, N Franck, H Duval, M Roussel, B Guillet

引用次数: 0

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