Niedbala W, Wei X Q, Piedrafita D, Xu D, Liew F Y
Department of Immunology, University of Glasgow, Glasgow, GB.
Eur J Immunol. 1999 Aug;29(8):2498-505. doi: 10.1002/(SICI)1521-4141(199908)29:08<2498::AID-IMMU2498>3.0.CO;2-M.
We have previously shown that mice lacking inducible NO synthase are markedly more susceptible to Leishmania major infection but developed a significantly enhanced Th1 cell response compared with wild-type mice. Furthermore, at high concentrations, NO inhibited IL-12 synthesis by activated macrophages, thereby indirectly suppressing the expansion of Th1 cells. We report here that at low concentrations, NO selectively enhanced the induction of Th1 cells and had no effect on Th2 cells. NO exerted this effect in synergy with IL-12 during Th1 cell differentiation and had no effect on fully committed Th1 cells. NO appears to affect CD4(+) T cells directly and not at the antigen-presenting cells. These results therefore provide an additional pathway by which NO modulates the immune response and contributes to the homeostasis of the immune system.
我们先前已表明，缺乏诱导型一氧化氮合酶的小鼠对硕大利什曼原虫感染明显更易感，但与野生型小鼠相比，其Th1细胞反应显著增强。此外，在高浓度时，一氧化氮抑制活化巨噬细胞合成IL-12，从而间接抑制Th1细胞的扩增。我们在此报告，在低浓度时，一氧化氮选择性增强Th1细胞的诱导，对Th2细胞无影响。在Th1细胞分化过程中，一氧化氮与IL-12协同发挥此作用，对完全分化的Th1细胞无影响。一氧化氮似乎直接影响CD4(+) T细胞，而不是抗原呈递细胞。因此，这些结果提供了一氧化氮调节免疫反应并有助于免疫系统稳态的另一条途径。
