Nickerson P, Zheng X X, Steiger J, Steele A W, Steurer W, Roy-Chaudhury P, Müller W, Strom T B
Harvard Medical School, Department of Medicine, Beth Israel Hospital, Boston, Massachusetts 02215, USA.
Transpl Immunol. 1996 Mar;4(1):81-5. doi: 10.1016/s0966-3274(96)80043-8.
Murine CTLA4/Fc therapy leads to permanent engraftment of islet allografts in interleukin 4 (IL-4) knockout (IL-4-/- mice. Interestingly, IL-4+/- hosts were more resistant to tolerance induction than IL-4-/- mice. An IL-2/Fc fusion protein abrogates the effect of CTLA4/Fc therapy while an IL-4/Fc fusion protein tends to inhibit rather than enhance the effect of CTLA/Fc treatment in IL-4-/- recipients. We conclude that allograft acceptance requires principally a blockade of T cell activation rather than 'immune deviation' of the T cell activation program to Th2 cytokines (i.e. IL-4).
小鼠CTLA4/Fc疗法可使胰岛同种异体移植物在白细胞介素4（IL-4）基因敲除（IL-4-/-）小鼠中永久植入。有趣的是，与IL-4-/-小鼠相比，IL-4+/-宿主对诱导耐受更具抗性。IL-2/Fc融合蛋白可消除CTLA4/Fc疗法的效果，而IL-4/Fc融合蛋白在IL-4-/-受体中倾向于抑制而非增强CTLA/Fc治疗的效果。我们得出结论，同种异体移植物的接受主要需要阻断T细胞活化，而非将T细胞活化程序“免疫偏离”为Th2细胞因子（即IL-4）。
