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[MRL lpr/lpr→MRL +/+]嵌合体中消瘦综合征与[B10.D2→BALB/c]嵌合体中移植物抗宿主病的比较以及将[MRL lpr/lpr→MRL +/+]中的消瘦综合征转移至MRL +/+小鼠的尝试。

Comparison of wasting syndrome in [MRL lpr/lpr-->MRL +/+] chimera and graft versus host disease in [B10.D2-->BALB/c] chimera and an attempt to transfer the wasting syndrome in [MRL lpr/lpr-->MRL +/+] to MRL +/+ mice.

作者信息

Aihara M, Aihara Y, Nakajima H

机构信息

Department of Dermatology, Yokohama City University School of Medicine, Japan.

出版信息

J Dermatol Sci. 1994 Apr;7(2):107-18. doi: 10.1016/0923-1811(94)90084-1.

Abstract

We compared the findings in the wasting syndrome seen in [MRL lpr/lpr--> MRL +/+] chimeras with those of chronic graft versus host disease (GVHD) in [B10.D2-->BALB/c] chimeras. BALB/c mice were lethally irradiated and administered B10.D2 spleen and bone marrow cells. These mice are identical to MHC and Mls but differ as to genetic background. As a result of chronic GVHD, these [B10.D2-->BALB/c] chimeras showed hair loss, weight loss and atrophy of lymph nodes and spleen beginning 5 weeks after the transplantation. MRL lpr/lpr mice carry the lpr gene and spontaneously develop generalized lymph node swelling and lupus-like autoimmune disease, while congenic MRL +/+ mice lack the lpr gene. The [MRL lpr/lpr-->MRL +/+] chimeras showed wasting and the same symptoms as in [B10.D2-BALB/c] chimeras beginning 16 weeks after cell transfer. Skin biopsy from both chimeras showed very similar changes on HE staining and on immunoperoxidase staining for Ia and Thy-1. Our data suggest that very small differences in minor histocompatibility may induce GVHD which produces severe wasting with lethal consequences. Finally, we succeeded in transferring the wasting syndrome seen in the [MRL lpr/lpr--> MRL +/+] chimera to other MRL +/+ mice by transplanting spleen cells from the [MRL lpr/lpr-->MRL +/+] chimera to lethally irradiated MRL +/+ mice.

摘要

我们将[MRL lpr/lpr→MRL +/+]嵌合体中出现的消瘦综合征的研究结果与[B10.D2→BALB/c]嵌合体中慢性移植物抗宿主病(GVHD)的研究结果进行了比较。对BALB/c小鼠进行致死性照射,并给予B10.D2脾细胞和骨髓细胞。这些小鼠的主要组织相容性复合体(MHC)和次要淋巴细胞刺激抗原(Mls)相同,但遗传背景不同。由于慢性GVHD,这些[B10.D2→BALB/c]嵌合体在移植后5周开始出现脱发、体重减轻以及淋巴结和脾脏萎缩。MRL lpr/lpr小鼠携带lpr基因,会自发出现全身性淋巴结肿大和狼疮样自身免疫性疾病,而同基因的MRL +/+小鼠则缺乏lpr基因。[MRL lpr/lpr→MRL +/+]嵌合体在细胞移植后16周开始出现消瘦以及与[B10.D2 - BALB/c]嵌合体相同的症状。对两种嵌合体进行皮肤活检,苏木精-伊红(HE)染色以及Ia和Thy-1的免疫过氧化物酶染色显示出非常相似的变化。我们的数据表明,次要组织相容性方面的微小差异可能会诱发GVHD,进而导致严重消瘦并产生致命后果。最后,我们通过将[MRL lpr/lpr→MRL +/+]嵌合体的脾细胞移植到经致死性照射的MRL +/+小鼠体内,成功地将[MRL lpr/lpr→MRL +/+]嵌合体中出现的消瘦综合征转移到了其他MRL +/+小鼠身上。

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