Pathogenesis of herpes simplex virus-induced ocular immunoinflammatory lesions in B-cell-deficient mice
Pathogenesis of herpes simplex virus-induced ocular immunoinflammatory lesions in B-cell-deficient mice
复制标题
DOI：
10.1128/jvi.74.8.3517-3524.2000
复制
发表时间：
2000-04-01
影响因子：
5.4
通讯作者：
Rouse, BT
中科院分区：
文献类型：
--
作者：
Deshpande, SP;Zheng, M;Rouse, BT
用免疫球蛋白IJ研究了B细胞和体液免疫在单纯疱疹病毒（HSV）眼部感染中的作用。链基因靶向的B细胞缺陷小鼠（μ K/O），在免疫活性小鼠良好耐受的病毒剂量下，观察到μ K/O小鼠对疱疹性脑炎以及疱疹性基质角膜炎（HSK）的易感性增加。对mu K/O小鼠中HSK严重程度增加的原因进行了解释。首先，mu K/O小鼠缺乏抗体应答导致病毒持续时间更长，并传播到角膜基质（炎症部位）。病毒在角膜基质中的长期表达可能导致Th 1型CD 4 + T细胞的旁观者激活，进一步导致mu K/O小鼠HSK病变表达的严重性。其次，与野生型小鼠相比，mu K/O小鼠产生最小的Th 2细胞因子应答，这种应答可能有助于下调Th 1介导的HSR病变的严重性。
The role of B cells and humoral immunity in herpes simplex virus (HSV) ocular infections was studied in immunoglobulin IJ. chain gene-targeted B-cell-deficient mice (mu K/O), At doses of virus well tolerated by immunocompetent mice, heightened susceptibility of mu K/O mice to herpetic encephalitis as well as to herpetic stromal keratitis (HSK) was observed. An explanation was sought for the increased severity of HSK in the mu K/O mice. First, the lack of antibody responses in mu K/O mice resulted in longer viral persistence and dissemination to the corneal stroma, the site of inflammation. Prolonged virus expression in the corneal stroma was suggested to cause bystander activation of Th1-type CD4+ T cells, further contributing to the severity of HSK lesion expression in mu K/O mice, Second, mu K/O mice generated minimal Th2 cytokine responses compared to wild-type mice, Such responses might serve to downregulate the severity of Th1-mediated HSR lesions.