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细胞毒性T淋巴细胞对B细胞肿瘤上与免疫球蛋白重链(Igh)相关的组织相容性抗原H-40的识别。

Recognition of an Igh-linked histocompatibility antigen, H-40, on B-cell tumors by cytotoxic T lymphocytes.

作者信息

Forman J, Ciavarra R, Henderson L A

出版信息

Surv Immunol Res. 1985;4(1):41-7. doi: 10.1007/BF02918585.

Abstract

This article reviews our data on H-40, a histocompatibility antigen controlled by a locus linked to Igh structural genes but telomeric to Tsu. The antigen is detected by rejection of H-40+ tumor cells in vivo and by the activity of H-2 restricted anti-H-40 cytotoxic T lymphocytes in vitro. H-40 is expressed on lipopolysaccharide stimulated B cells and B cell tumors that express surface(s) IgM and not on sIgM- tumors or other neoplastic cells. Its expression on the sIgM,D+ BALB/c (Igha, H-40a) derived leukemia, BCL1, prevents its transplantability across the Ig heavy chain (and H-40) barrier into C.B-20 (Ighb, H-40b) mice; whereas, BALB/c tumors that do not express H-40 can be transplanted into this allotype-congenic recipient. Although irradiated C.B-20 animals are susceptible to the BCL1 tumor, adoptive transfer of a mixture of Lyt-2+ and Lyt-2- effector cells (anti-H-40) from C.B-20 animals that have previously rejected BCL1 protect such recipients. However, the same effector cells will not protect irradiated BALB/c or (BALB/c X C.B-20)F1 recipients from this tumor. Since normal BALB/c sIg+ cells express H-40, either the effector cells are diverted from interacting with and destroying the tumor, or recognition of H-40 on non-tumor cells elicits a suppressor mechanism.

摘要

本文回顾了我们关于H - 40的研究数据,H - 40是一种组织相容性抗原,由与Igh结构基因连锁但位于Tsu端粒侧的一个基因座所控制。该抗原可通过体内对H - 40+肿瘤细胞的排斥反应以及体外H - 2限制的抗H - 40细胞毒性T淋巴细胞的活性来检测。H - 40在脂多糖刺激的B细胞以及表达表面IgM的B细胞肿瘤上表达,而在sIgM - 肿瘤或其他肿瘤细胞上不表达。它在源自sIgM、D + BALB/c(Igha,H - 40a)的白血病BCL1上的表达,阻止了其跨越Ig重链(和H - 40)屏障移植到C.B - 20(Ighb,H - 40b)小鼠体内;然而,不表达H - 40的BALB/c肿瘤可以移植到这种同种异型基因的受体小鼠体内。尽管经辐射的C.B - 20动物对BCL1肿瘤易感,但先前已排斥BCL1的C.B - 20动物的Lyt - 2+和Lyt - 2 - 效应细胞(抗H - 40)混合物的过继转移可保护此类受体。然而,相同的效应细胞不能保护经辐射的BALB/c或(BALB/c×C.B - 20)F1受体免受该肿瘤的侵害。由于正常的BALB/c sIg+细胞表达H - 40,要么效应细胞被转移而无法与肿瘤相互作用并将其破坏,要么对非肿瘤细胞上H - 40的识别引发了一种抑制机制。

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