Importance of hepatic lymphocytes on innate immunity

疟疾寄生虫是细胞内的病原体，因此侵入红细胞和肝细胞。在这方面，传统的T和B细胞不能抵抗寄生虫。相反，胸腺外T细胞和B-1细胞通过自身反应和自身抗体攻击这种寄生虫。这些证据在小鼠和人体研究中都得到了证实。我们还发现，疟疾感染后小鼠的肝脏中可以诱导红细胞生成。据推测，肝脏中产生的新鲜红细胞可能是寄生虫的重要目标。TAP-1(-/-)缺失自我的小鼠也被用于研究，这些小鼠胸腺外T细胞丰富。胸腺外T细胞介导的先天免疫被发现对消除自我缺失具有重要意义。类似的现象也出现在应激小鼠和淀粉样变性小鼠身上。与胸腺外T细胞和B-1细胞一样，粒细胞也很重要。2004年，将抗促红细胞生成素抗体注射到患有疟疾的小鼠体内，发现可以治愈疟疾。2005年最后一年，α-GalCer激活NKT细胞导致肝功能衰竭。这一结果表明，NKT细胞的过度激活能够引起组织损伤。在疟疾感染中，NK1.1-TCR^和INT&GT；细胞也被发现是主要的淋巴细胞亚群。

Malarial parasites are intracellular pathogens and therefore invade erythrocytes and hepatocytes. In this respect, conventional T and B cells could not function against the parasites. Inversely, extrathymic T cells and B-1 cells attack such parasites by their autoreactivity and autoantibodies. These evidences were produced in both murine and human studies. We also found that erythropoiesis was induced in the liver of mice after malarial infection. It is speculated that fresh erythrocytes produced in the liver might be an important target for the parasites. TAP-1(-/-) mice with missing self were also used in this study and extrathymic T cells were abundant in these mice. Innate immunity mediated by extrathymic T cells is found to be importance to eliminate missing self. A similar phenomenon was also seen in mice with stress and in mice with amyloidosis. Granulocytes are also important in parallel with extrathymic T cells and B-1 cells. In 2004, anti-erythropoietin antibody was found to cure malaria when injected into mice with malaria. In 2005 final year, the activation of NKT cells by α-GalCer induced hepatic failure. This result indicated that overactivation of NKT cells is able to induce tissue damage. NK1.1-TCR^<int> cells are also found to be a major lymphocyte subset in malarial infection.