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荷瘤小鼠血清中可溶性低亲和力Fcγ受体(IgG结合因子)水平升高。

Increased levels of soluble low-affinity Fc gamma receptors (IgG-binding factors) in the sera of tumour-bearing mice.

作者信息

Lynch A, Tartour E, Teillaud J L, Asselain B, Fridman W H, Sautès C

机构信息

INSERM U.255, Institut Curie, Paris, France.

出版信息

Clin Exp Immunol. 1992 Feb;87(2):208-14. doi: 10.1111/j.1365-2249.1992.tb02976.x.

Abstract

Soluble forms of low affinity Fc gamma receptors (Fc gamma R), also called IgG-binding factors (IgG-BF), have been shown to play a regulatory role in immune responses. By using an immunodot assay with the anti-mouse Fc gamma R MoAb, 2.4G2, the levels of IgG-BF have been measured in the sera of mice bearing syngeneic tumours of lymphoid or non-lymphoid origin or in mice injected with high doses of murine IgG. These sera contained large amounts of IgG-BF as compared with controls. In the case of mice bearing IgG2a- or IgG2b-secreting hybridomas or lymphomas, serum IgG-BF increased progressively with tumour size and serum monoclonal IgG concentration, reaching 4-12 times the normal levels. A less than three-fold increase was found in mice bearing an IgG1-secreting hybridoma or tumours which do not secrete IgG (IgA-secreting hybridoma, non-immunoglobulin-secreting lymphoid tumours or melanoma) or in mice injected with 9 mg of monoclonal IgG2a. The enhancement of serum IgG-BF levels was independent of the expression of Fc gamma R by the tumour cells, suggesting that the majority of IgG-BF secreted in response to tumours was produced by the host rather than by the tumour. The increased production of IgG-BF may participate in the control of tumour growth and in the modulation of the host immune responses in tumour-bearing animals.

摘要

低亲和力Fcγ受体(FcγR)的可溶性形式,也称为IgG结合因子(IgG-BF),已被证明在免疫反应中起调节作用。通过使用抗小鼠FcγR单克隆抗体2.4G2进行免疫斑点测定,已测量了患有同基因淋巴样或非淋巴样起源肿瘤的小鼠血清中或注射高剂量小鼠IgG的小鼠血清中IgG-BF的水平。与对照组相比,这些血清含有大量的IgG-BF。在患有分泌IgG2a或IgG2b的杂交瘤或淋巴瘤的小鼠中,血清IgG-BF随着肿瘤大小和血清单克隆IgG浓度的增加而逐渐升高,达到正常水平的4至12倍。在患有分泌IgG1的杂交瘤或不分泌IgG的肿瘤(分泌IgA的杂交瘤、不分泌免疫球蛋白的淋巴样肿瘤或黑色素瘤)的小鼠中,或在注射9mg单克隆IgG2a的小鼠中,发现增加不到三倍。血清IgG-BF水平的升高与肿瘤细胞FcγR的表达无关,这表明响应肿瘤分泌的大多数IgG-BF是由宿主而非肿瘤产生的。IgG-BF产量的增加可能参与了肿瘤生长的控制以及荷瘤动物宿主免疫反应的调节。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c256/1554268/60f67b61f211/clinexpimmunol00052-0044-a.jpg

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