In vivo and in vitro induction of class II molecules on canine renal cells and their effect on the mixed lymphocyte kidney cell culture.

In vivo and in vitro induction of class II molecules on canine renal cells and their effect on the mixed lymphocyte kidney cell culture.
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II类分子对犬肾细胞的体内和体外诱导及其对混合淋巴细胞肾细胞培养物的影响。

DOI:
10.1097/00007890-198711000-00017
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发表时间:
1987
期刊:
影响因子:
6.2
通讯作者:
Miller,J
Miller,J
中科院分区:
医学2区
文献类型:
--
作者:
Esquenazi,V;Fuller,L;Pardo,V;Roth,D;Milgrom,M;Miller,J

文献摘要

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犬肾皮质细胞是通过胶原酶从同种异体半相合、供受体配对和无血缘关系的杂种中分离获得的。在混合淋巴细胞肾细胞培养(MLKC)中,来自正常和排斥移植肾的肾皮质细胞也刺激了杂交狗以及表现出高淋巴细胞培养(MLC)反应的Beagle对中的一个成员的外周血淋巴细胞(PBL)。正常肾皮质细胞出现中等程度的自体MLKC反应性。然而,排斥的肾皮质细胞在同种异体和自体MLKC反应中明显比正常肾皮质细胞更具刺激性。供体动物的淋巴细胞对移植排斥反应期间分离的自体皮质细胞的反应比对正常同种异体肾脏的皮质细胞反应更强烈。从排斥肾中提取的受者浸润性淋巴细胞和增殖的T细胞系对来自该肾的皮质细胞的反应也比PBL更强。免疫组织化学染色和电子显微镜显示,刺激的皮质细胞的梯度纯化导致一种几乎纯的远端肾小管上皮细胞的制备,这导致对MLKC的刺激增强。
Canine renal cortical cells were obtained by collagenase extraction from allogeneic haploidentical, donor-recipient beagle littermate pairs and from unrelated mongrels. Peripheral blood lymphocytes (PBL) of the mongrels, as well as of one member of the beagle pair that exhibited high mined lymphocyte culture (MLC) reactivity against the other were also stimulated by renal cortical cells derived from both normal and rejected transplanted kidneys in mixed lymphocyte kidney cell culture (MLKC). A moderate autologous MLKC reactivity occurred in response to normal renal cortical cells. However, rejected kidney cortical cells were markedly more stimulatory than normal renal cortical cells in both allogeneic and autologous MLKC reactions. Lymphocytes from donor animals responded more strongly to autologous cortical cells isolated during rejection of the transplant than to cortical cells from normal allogeneic kidneys. Recipient infiltrating lymphocytes and propagated T cell lines extracted from the rejected kidney also responded more strongly than PBL to cortical cells from this kidney. Gradient purification of the stimulating cortical cells resulted in one virtually pure preparation of distal tubular epithelial cells, as demonstrated by immunohistochemical stains and electron microscopy, which caused enhanced stimulation in MLKC.