Genetic control of immunity to Trichinella spiralis infections of mice. Hypothesis to explain the role of H-2 genes in primary and challenge infections.
Genetic control of immunity to Trichinella spiralis infections of mice. Hypothesis to explain the role of H-2 genes in primary and challenge infections.
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发表时间：
1984-04
期刊：
影响因子：
6.4
通讯作者：
D. L. Wassom;D. Wakelin;Bradford O. Brooks;C. Krco;C. David
中科院分区：
文献类型：
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作者：
D. L. Wassom;D. Wakelin;Bradford O. Brooks;C. Krco;C. David
H-2同源品系小鼠的排T能力进行了比较。螺旋体感染从小肠和他们的能力，以限制繁殖的成年女性蠕虫。B10.M小鼠（H-2f）比菌株B10.Q（H-2 q）和B10.BR（H-2k）更快地排出原发感染和攻毒感染。在初次感染期间，B10.M小鼠在感染后第9天之前开始排出蠕虫，并且在第12天和第15天，蠕虫计数与B10.BR小鼠中的计数显著不同（P小于0.05学生t检验）。B10.Q小鼠排出蠕虫比B10.BR更快，但蠕虫计数直到第15天才显著不同。虽然B10.M小鼠对从肠道中排出蠕虫的反应最快，但B10.Q小鼠在限制蠕虫繁殖方面最有效。从B10.Q小鼠收获的雌性蠕虫在体外培养24小时产生的新生幼虫显著少于B10.M或B10.BR小鼠的蠕虫。来自B10.M小鼠的蠕虫的繁殖力低于来自B10.BR的蠕虫，但在感染后第9天之前，这种差异不明显，并且来自B10.M的蠕虫总是比来自B10.Q的蠕虫繁殖力更高。在200 T预激剂量后21天进行攻毒感染。旋毛虫肌幼虫很快被排斥。B10.M小鼠在前24小时内排出65%的蠕虫。到攻毒后第6天，B10.M小鼠已排出84%的蠕虫; B10.Q和B10.BR分别排出75%和37%。这些结果表明，快速驱逐反应可能在许多不同品系的小鼠中表达，这取决于小鼠的免疫方式和感染剂量的大小。与初次感染对照相比，所有供试菌株在攻毒感染后6天雌性蠕虫的繁殖力均降低;然而，B10.Q小鼠的蠕虫繁殖力低于B10.M或B10.BR小鼠的蠕虫。这些实验的结果表明，H-2基因在控制将蠕虫从肠道排出的免疫应答和限制蠕虫繁殖的应答中起重要作用。这些H-2控制的差异在初次感染和攻毒感染期间均表达。由于目前的结果与其他地方发表的结果有些冲突，我们提出了一个新的假设来解释迄今为止在我们实验室收集的数据。根据这一假说，抗成虫反应，抗繁殖反应，快速驱逐反应是独立的遗传控制下，并受到H-2和非H-2基因的相互作用的产物。
H-2 congenic strains of mice were compared for their ability to expel T. spiralis infections from the small intestine and for their ability to limit the reproduction of adult female worms. B10.M mice (H-2f) expelled both primary and challenge infections more quickly than did the strains B10.Q(H-2q) and B10.BR(H-2k). During a primary infection, expulsion of worms from B10.M mice began before Day 9 post-infection and worm counts differed significantly (P less than .05 Student's t-test) from counts in B10.BR mice on each of Days 12 and 15.B10.Q mice expelled worms more rapidly than B10.BR but worm counts did not differ significantly until Day 15. Whereas B10.M mice responded most quickly to expel worms from the gut, B10.Q mice were most effective in limiting worm reproduction. Female worms harvested from B10.Q mice and cultured for 24 hr in vitro produced significantly fewer newborn larvae than did worms from B10.M or B10.BR mice. Worms from B10.M mice were less fecund than worms from B10.BR, but this difference was not apparent before Day 9 post-infection, and worms from B10.M were always more fecund than worms from B10.Q. Challenge infections 21 days following a priming dose of 200 T. spiralis muscle larvae were rejected very quickly. B10.M mice expelled 65% of their worms during the first 24 h. By Day 6 after challenge, B10.M mice had expelled 84% of their worms; B10.Q and B10.BR expelled 75% and 37% respectively. These results suggest that a rapid expulsion response may be expressed in many different strains of mice depending on how the mice are immunized and the size of the infecting dose. Fecundity of female worms 6 days following a challenge infection was reduced for all strains tested when compared to primary infection controls; however, worms from B10.Q mice were less fecund than worms from B10.M or B10.BR. Results of these experiments demonstrate that H-2 genes play an important role in controlling the immune response which expels worms from the gut and the response which limits worm reproduction. These H-2-controlled differences are expressed during both primary and challenge infections. As the present results conflict somewhat with results published elsewhere, we have proposed a new hypothesis to explain the data collected in our laboratories thus far. According to this hypothesis, the anti-adult response, the anti-fecundity response, and the rapid expulsion response are under independent genetic control and influenced by the interacting products of both H-2 and non-H-2 genes.