Heinzel F P, Rerko R M, Hujer A M, Maier R A
Division of Geographic Medicine, Case Western Reserve University School of Medicine, and the VA Medical Center, Cleveland, Ohio 44106, USA.
Infect Immun. 1998 Sep;66(9):4537-40. doi: 10.1128/IAI.66.9.4537-4540.1998.
Lymph node cells of BALB/c mice with progressive leishmaniasis produced sixfold more interleukin-2 (IL-2) in culture than those of healing C57BL/6 mice. IL-2 synthesis also increased in C57BL/6 mice made susceptible by IL-12 or gamma interferon deficiency. However, IL-2 mRNA levels in vivo did not reflect IL-2 production in vitro. Because IL-2 contributes to the pathogenesis of progressive leishmaniasis, the functional significance of these findings should be further explored.
患有进行性利什曼病的BALB/c小鼠的淋巴结细胞在培养物中产生的白细胞介素-2(IL-2)比正在康复的C57BL/6小鼠的淋巴结细胞多五倍。在因IL-12或γ干扰素缺乏而变得易感的C57BL/6小鼠中,IL-2的合成也增加了。然而,体内IL-2 mRNA水平并未反映体外IL-2的产生情况。由于IL-2促成了进行性利什曼病的发病机制,这些发现的功能意义应进一步探究。