Li S L, Kaaya E E, Feichtinger H, Putkonen P, Parravicini C, Böttiger D, Biberfeld G, Biberfeld P
Immunopathology Lab., Karolinska Institute, Stockholm, Sweden.
Res Virol. 1991 Mar-Jun;142(2-3):173-82. doi: 10.1016/0923-2516(91)90054-7.
A non-opportunistic, generalized giant cell disease (GCD) was found in 12 out of 25 (48%) cynomologus monkeys infected with SIVsm. Most organs were affected notably the lymph nodes (LN), spleen, gut, liver, lungs and CNS. The multinucleated GC varied considerably in cell size and in the number and cytoplasmic distribution of the nuclei. Immunohistochemically most GC expressed SIV antigens and markers of mononuclear phagocytes (CD68), CD4 and also occasionally the T-cell markers CD45RO, CD43 and CD2. Monkeys with GCD had more pronounced immunosuppression with lower CD4-cell counts, more often demonstrable SIV antigen in the blood and LN and had been infected for a longer time period, as compared to monkeys without GCD. These findings show that SIV infection in cynomolgus monkeys is frequently associated with extensive formation of multinucleated GC of macrophage origin, which appears to be related to the pathogenesis of the infection and the degree of immunosuppression.
在感染了SIVsm的25只食蟹猴中，有12只（48%）发现了一种非机会性的全身性巨细胞疾病（GCD）。大多数器官都受到影响，尤其是淋巴结（LN）、脾脏、肠道、肝脏、肺和中枢神经系统。多核巨细胞在细胞大小以及细胞核的数量和胞质分布方面差异很大。免疫组织化学显示，大多数巨细胞表达SIV抗原和单核吞噬细胞标志物（CD68）、CD4，偶尔也表达T细胞标志物CD45RO、CD43和CD2。与没有GCD的猴子相比，患有GCD的猴子免疫抑制更为明显，CD4细胞计数更低，血液和淋巴结中更常检测到SIV抗原，并且感染时间更长。这些发现表明，食蟹猴感染SIV常与巨噬细胞来源的多核巨细胞广泛形成有关，这似乎与感染的发病机制和免疫抑制程度有关。
