The role of cell-mediated cytotoxicity in acute GVHD after MHC-matched allogeneic bone marrow transplantation in mice.
The role of cell-mediated cytotoxicity in acute GVHD after MHC-matched allogeneic bone marrow transplantation in mice.
复制标题
DOI：
10.1084/jem.183.6.2645
复制
发表时间：
1996-06-01
期刊：
影响因子：
--
通讯作者：
Levy RB
中科院分区：
文献类型：
--
作者：
Baker MB;Altman NH;Podack ER;Levy RB
细胞介导的细胞毒性在移植物抗宿主病（GVHD）的复杂病理生理学中的作用几十年来一直定义不清。我们将Fas配体（FasL）缺陷和穿孔素缺陷突变供体小鼠的T细胞移植到致死性照射的MHC匹配的同种异体受体小鼠中，以表征细胞介导的细胞毒性在GVHD中的作用。尽管同种异体FasL缺陷型供体T细胞的受体经历了严重的GVHD相关恶病质，但它们仅表现出肝脏和皮肤GVHD病理学的最小体征。接受穿孔素缺陷的同种异体供体T细胞的受者出现了急性GVHD的迹象，但发病时间明显延迟。这些发现表明Fas介导的抗受体细胞毒性可能对肝脏和皮肤GVHD的发展至关重要，但不是GVHD相关恶病质所必需的。此外，穿孔素介导的抗受体细胞毒性似乎在GVHD病理生理学的动力学中起重要作用，但不是GVHD相关组织损伤所必需的。
The role of cell-mediated cytotoxicity in the complex pathophysiology of graft-versus-host disease (GVHD) has remained poorly defined for several decades. We transplanted T cells from Fas-ligand (FasL)- defective and perforin-deficient mutant donor mice into lethally irradiated MHC-matched allogeneic recipient mice to characterize the role of cell-mediated cytotoxicity in GVHD. Although recipients of allogeneic FasL-defective donor T cells underwent severe GVHD- associated cachexia, they exhibited only minimal signs of hepatic and cutaneous GVHD pathology. Recipients of perforin-deficient allogeneic donor T cells developed signs of acute GVHD, but the time of onset was significantly delayed. These findings demonstrate that Fas-mediated anti-recipient cytotoxicity may be critical for the development of hepatic and cutaneous GVHD, but is not required for GVHD-associated cachexia. In addition, perforin-mediated anti-recipient cytotoxicity appears to play an important role in the kinetics of GVHD pathophysiology, but is not required for GVHD-associated tissue damage.
登录
查看更多内容
DOI：
10.1084/jem.172.5.1367
发表时间：
1990-11-01
期刊：
The Journal of experimental medicine
影响因子：
--
作者：
Allen RD;Marshall JD;Roths JB;Sidman CL
通讯作者：
Sidman CL
影响因子：
5.6
作者：
GALLUCCI, BB;EPSTEIN, R;THOMAS, ED
通讯作者：
THOMAS, ED
影响因子：
6.5
作者：
SAYAMA, K;YONEHARA, S;MIKI, Y
通讯作者：
MIKI, Y
影响因子：
64.8
作者：
KAGI, D;LEDERMANN, B;HENGARTNER, H
通讯作者：
HENGARTNER, H
影响因子：
64.8
作者：
LOWIN, B;HAHNE, M;TSCHOPP, J
通讯作者：
TSCHOPP, J