对幽门螺杆菌感染的显性无反应性与白细胞介素10的产生有关，而与γ干扰素无关。
Dominant nonresponsiveness to Helicobacter pylori infection is associated with production of interleukin 10 but not gamma interferon.
作者信息
Sutton P, Kolesnikow T, Danon S, Wilson J, Lee A
机构信息
School of Microbiology and Immunology, University of New South Wales, Sydney, New South Wales 2052, Australia.
出版信息
Infect Immun. 2000 Aug;68(8):4802-4. doi: 10.1128/IAI.68.8.4802-4804.2000.
Abstract
Helicobacter pylori-induced gastritis is an essential precursor lesion for the development of peptic ulcers or gastric adenocarcinoma. We demonstrate that nonresponsiveness to H. pylori SS1 infection is dominantly inherited in mice. F(1) hybrid crosses between a nonresponder mouse and three responder strains all possessed the nonresponder phenotype. Secretion of interleukin-10 but not gamma interferon was associated with nonresponsiveness to infection.
摘要
幽门螺杆菌诱导的胃炎是消化性溃疡或胃腺癌发生的重要前期病变。我们证明，对幽门螺杆菌SS1感染无反应性在小鼠中呈显性遗传。无反应性小鼠与三个有反应性品系之间的F(1)杂种杂交后代均具有无反应性表型。白细胞介素-10而非γ干扰素的分泌与对感染的无反应性相关。
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A genetic basis for atrophy: dominant non-responsiveness and helicobacter induced gastritis in F(1) hybrid mice.萎缩的遗传基础：F1 杂交小鼠中的显性无反应性和幽门螺杆菌诱导的胃炎
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