BackgroundThe pathogenesis of immunological tolerance caused by avian leukosis virus subgroup J (ALV-J), an oncogenic retrovirus, is largely unknown.ResultsIn this study, the development, differentiation, and immunological capability of B cells and their progenitors infected with ALV-J were studied both morphologically and functionally by using a model of ALV-J congenital infection. Compared with posthatch infection, congenital infection of ALV-J resulted in severe immunological tolerance, which was identified as the absence of detectable specific antivirus antibodies. In congenitally infected chickens, immune organs, particularly the bursa of Fabricius, were poorly developed. Moreover, IgM-and IgG-positive cells and total immunoglobulin levels were significantly decreased in these chickens. Large numbers of bursa follicles with no differentiation into cortex and medulla indicated that B cell development was arrested at the early stage. Flow cytometry analysis further confirmed that ALV-J blocked the differentiation of CD117+chB6+ B cell progenitors in the bursa of Fabricius. Furthermore, both the humoral immunity and the immunological capability of B cells and their progenitors were significantly suppressed, as assessed by (a) the antibody titres against sheep red blood cells and the Marek’s disease virus attenuated serotype 1 vaccine; (b) the proliferative response of B cells against thymus-independent antigen lipopolysaccharide (LPS) in the spleen germinal centres; and (c) the capacities for proliferation, differentiation and immunoglobulin gene class-switch recombination of B cell progenitors in response to LPS and interleukin-4(IL-4) in vitro.ConclusionsThese findings suggested that the anergy of B cells in congenitally infected chickens is caused by the developmental arrest and dysfunction of B cell progenitors, which is an important factor for the immunological tolerance induced by ALV-J.

中文翻译：

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禽白血病病毒J亚群诱导CD117+chB6+B细胞祖细胞克隆无反应性与免疫耐受相关

背景禽白血病病毒亚群J（ALV-J）是一种致癌逆转录病毒，引起免疫耐受的发病机制尚不清楚。结果本研究中，感染ALV-J的B细胞及其祖细胞的发育、分化和免疫能力均未明确。通过使用 ALV-J 先天性感染模型对形态和功能进行了研究。与孵化后感染相比，先天性 ALV-J 感染导致严重的免疫耐受，这被确定为缺乏可检测的特异性抗病毒抗体。先天性感染鸡的免疫器官，尤其是法氏囊，发育不良。此外，这些鸡的 IgM 和 IgG 阳性细胞和总免疫球蛋白水平显着降低。大量未分化为皮质和髓质的法氏囊滤泡表明 B 细胞发育在早期停滞。流式细胞术分析进一步证实ALV-J阻断了法氏囊中CD117+chB6+B细胞祖细胞的分化。此外，B 细胞及其祖细胞的体液免疫和免疫能力均受到显着抑制，如 (a) 针对绵羊红细胞和马立克氏病病毒减毒血清 1 型疫苗的抗体滴度所评估的；(b) B 细胞在脾生发中心对胸腺非依赖性抗原脂多糖 (LPS) 的增殖反应；(c) 扩散能力，