Kanagawa O, Vaupel B A, Gayama S, Koehler G, Kopf M
Department of Pathology and Medicine, Washington University School of Medicine, St. Louis, MO 63110.
Science. 1993 Oct 8;262(5131):240-2. doi: 10.1126/science.8211142.
The murine acquired immunodeficiency syndrome (MAIDS) is induced by a defective murine leukemia virus and has many symptoms similar to those found in patients infected with the human immunodeficiency virus. The presence of both B cells and CD4+ T cells is critical for the development of the disease. Furthermore, a Th2 cytokine response dominates during the progression of the disease. When interleukin-4 (IL-4)-deficient mice that are defective in Th2 cytokine responses were infected, there was no lethality, and the development of the T cell abnormalities associated with MAIDS was delayed. These data suggest that IL-4 or a Th2 response is involved in the development of retrovirus-induced immunodeficiency in mice.
小鼠获得性免疫缺陷综合征（MAIDS）由一种缺陷型小鼠白血病病毒诱发，具有许多与人类免疫缺陷病毒感染患者相似的症状。B细胞和CD4+ T细胞的存在对该疾病的发展至关重要。此外，在疾病进展过程中，Th2细胞因子反应占主导地位。当感染了Th2细胞因子反应存在缺陷的白细胞介素-4（IL-4）缺陷小鼠时，未出现致死情况，且与MAIDS相关的T细胞异常发展有所延迟。这些数据表明，IL-4或Th2反应参与了小鼠逆转录病毒诱导的免疫缺陷的发展。
