Implicating a role for immune recognition of self in tumor rejection: passive immunization against the brown locus protein.

Implicating a role for immune recognition of self in tumor rejection: passive immunization against the brown locus protein.
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暗示了免疫识别自我在肿瘤排斥反应中的作用:针对棕色基因座蛋白的被动免疫。

DOI:
10.1084/jem.182.5.1609
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发表时间:
1995-11-01
影响因子:
15.3
通讯作者:
Houghton, Alan N.
Houghton, Alan N.
中科院分区:
医学1区
文献类型:
--
作者:
Hara, Isao;Takechi, Yoshizumi;Houghton, Alan N.

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免疫系统可以识别在恶性细胞及其正常细胞对应物上选择性表达的分化抗原。然而,对分化抗原的免疫是否能有效地导致肿瘤排斥还不确定。小鼠棕色基因座蛋白,gp 75或酪氨酸酶相关蛋白1,是黑色素瘤和正常黑色素细胞表达的黑色素细胞分化抗原。gp 75抗原被黑色素瘤患者的自身抗体和自身反应性T细胞识别。为了模拟针对黑素细胞分化抗原的自身免疫,将针对gp 75的小鼠抗体被动转移到荷瘤小鼠中。被动免疫小鼠单克隆抗体对gp 75诱导的保护和排斥的皮下肿瘤和肺转移在同基因C57 BL/6小鼠,包括建立的肿瘤。被动免疫产生毛色改变,但仅在再生毛。该系统为自身免疫性白癜风提供了一个模型,并表明对黑素细胞分化抗原的免疫反应可以影响小鼠毛色。黑素细胞分化抗原的免疫识别可以排斥肿瘤,为靶向癌症上表达的组织自身抗原提供了基础。
The immune system can recognize differentiation antigens that are selectively expressed on malignant cells and their normal cell counterparts. However, it is uncertain whether immunity to differentiation antigens can effectively lead to tumor rejection. The mouse brown locus protein, gp75 or tyrosinase-related protein 1, is a melanocyte differentiation antigen expressed by melanomas and normal melanocytes. The gp75 antigen is recognized by autoantibodies and autoreactive T cells in persons with melanoma. To model autoimmunity against a melanocyte differentiation antigen, mouse antibodies against gp75 were passively transferred into tumor-bearing mice. Passive immunization with a mouse monoclonal antibody against gp75 induced protection and rejection of both subcutaneous tumors and lung metastases in syngeneic C57BL/6 mice, including established tumors. Passive immunity produced coat color alterations but only in regenerating hairs. This system provides a model for autoimmune vitiligo and shows that immune responses to melanocyte differentiation antigens can influence mouse coat color. Immune recognition of a melanocyte differentiation antigen can reject tumors, providing a basis for targeting tissue autoantigens expressed on cancer.
DOI: 10.1038/newbio242148a0
发表时间: 1973-01-01
期刊: NATURE-NEW BIOLOGY
影响因子: --
作者:
FIDLER, IJ
通讯作者: FIDLER, IJ
DOI: 10.1084/jem.158.1.246
发表时间: 1983-07-01
期刊: The Journal of experimental medicine
影响因子: --
作者:
Naughton GK;Eisinger M;Bystryn JC
通讯作者: Bystryn JC
DOI: 10.1084/jem.179.3.1005
发表时间: 1994-03-01
期刊: The Journal of experimental medicine
影响因子: --
作者:
Bakker AB;Schreurs MW;de Boer AJ;Kawakami Y;Rosenberg SA;Adema GJ;Figdor CG
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DOI: 10.1073/pnas.85.12.4392
发表时间: 1988-06-01
影响因子: 11.1
作者:
JACKSON, IJ
通讯作者: JACKSON, IJ
DOI: 10.1111/1523-1747.ep12460906
发表时间: 1988-04-01
影响因子: 6.5
作者:
THOMSON, TM;REAL, FX;HOUGHTON, AN
通讯作者: HOUGHTON, AN