Rolland L, Ballet J J, Daniel-Ribeiro C
INSERM U 313, Groupe Hospitalier Pitié-Salpétriere, Paris, France.
Mem Inst Oswaldo Cruz. 1992 Apr-Jun;87(2):197-204. doi: 10.1590/s0074-02761992000200005.
In order to study the kinetics and composition of the polyclonal B-cell activation associated to malaria infection, antigen-specific and non-specific B-cell responses were evaluated in the spleens of mice infected with Plasmodium yoelii 17XL or injected with lysed erythrocytes or plasma from P. yoelii infected mice or with P. falciparum culture supernatants. Spleen/body weight ratio, numbers of nucleated spleen cells and Immunoglobulin-containing and Immunoglobulin-secreting cells increased progressively during the course of infection, in parallel to the parasitaemia. A different pattern of kinetics was observed when anti-sheep red blood cell and anti-trinitrophenylated-sheep red blood cell plaque forming cells response were studied: maximum values were observed at early stages of infection, whereas the number of total Immunoglobulin-containing and Immunoglobulin-secreting cells were not yet altered. Conversely, at the end of infection, when these latter values reached their maximum, the anti-sheep red blood cell and anti-trinitrophenylated-sheep red blood cell specific responses were normal or even infranormal. In mice injected with Plasmodium-derived material, a higher increase in antigen-specific PFC was observed, as compared to the increase of Immunoglobulin-containing and Immunoglobulin-secreting cell numbers. This suggested a "preferential" (antigen-plus mitogen-induced) stimulation of antigen-specific cells rather than a generalized non-specific (mitogen-induced) triggering of B-lymphocytes. On the basis of these and previous results, it is suggested that the polyclonal B-cell activation that takes place during the course of infection appears as a result of successive waves of antigen-specific B-cell activation.
为了研究与疟疾感染相关的多克隆B细胞活化的动力学和组成，在感染约氏疟原虫17XL的小鼠脾脏中，或注射约氏疟原虫感染小鼠的裂解红细胞、血浆，或注射恶性疟原虫培养上清液后，对抗抗原特异性和非特异性B细胞反应进行了评估。在感染过程中，脾/体重比、有核脾细胞数量以及含免疫球蛋白和分泌免疫球蛋白的细胞数量与寄生虫血症平行逐渐增加。当研究抗绵羊红细胞和抗三硝基苯化绵羊红细胞空斑形成细胞反应时，观察到不同的动力学模式：在感染早期观察到最大值，而此时含免疫球蛋白和分泌免疫球蛋白的细胞总数尚未改变。相反，在感染末期，当后者的值达到最大值时，抗绵羊红细胞和抗三硝基苯化绵羊红细胞特异性反应正常甚至低于正常水平。与注射疟原虫来源物质的小鼠相比，含免疫球蛋白和分泌免疫球蛋白的细胞数量增加时，抗原特异性PFC的增加更高。这表明是抗原特异性细胞的“优先”（抗原加丝裂原诱导）刺激，而不是B淋巴细胞的普遍非特异性（丝裂原诱导）触发。基于这些及以前的结果，提示感染过程中发生的多克隆B细胞活化似乎是抗原特异性B细胞活化连续波的结果。
