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致敏大鼠中载体特异性辅助性T细胞耐受性的诱导。

The induction of carrier-specific helper cell tolerance in presensitized rats.

作者信息

Sanfilippo F, Scott D W

出版信息

Eur J Immunol. 1977 May;7(5):283-7. doi: 10.1002/eji.1830070508.

DOI:10.1002/eji.1830070508
PMID:301476
Abstract

Lewis rats rendered tolerant to sheep IgG (SGG) show a markedly reduced antibody response to the 2,4,6-trinitrophenyl (TNP) hapten when later challenged with TNP-SGG. We have previously shown that this effect is due to functional unresponsiveness in the carrier SGG-specific helper T cell population. In this paper we demonstrate that induced helper cell tolerance is also maintained through a secondary immunogenic challenge. Furthermore, rats which are primed to the carrier SGG prior to tolerance induction also show a markedly reduced anti-TNP response upon secondary immunogenic challenge with TNP-SGG. The ability to specifically suppress a secondary response in this manner was found to be relatively long lasting, since rats showed reduced responsiveness when the secondary challenge was delayed for up to 4 weeks after tolerance induction. In addition, rats primed to the hapten (TNP) prior to carrier (SGG) tolerance induction also showed a marked reduction in anti-TNP antibody following challenge with TNP-SGG. These findings imply that helper cell tolerance can be induced in rats even after priming of carrier-specific (SGG) helper cells, or hapten-specific (TNP) B cells. These results parallel our other published findings that IgE responses in presensitized rats can be overcome by helper cell tolerance.

摘要

对绵羊免疫球蛋白G(SGG)产生耐受的刘易斯大鼠,在随后用三硝基苯(TNP)-SGG攻击时,对TNP半抗原的抗体反应明显降低。我们之前已经表明,这种效应是由于载体SGG特异性辅助性T细胞群体中的功能性无反应性所致。在本文中,我们证明诱导的辅助性细胞耐受也通过二次免疫原性攻击得以维持。此外,在诱导耐受之前对载体SGG进行致敏的大鼠,在用TNP-SGG进行二次免疫原性攻击时,其抗TNP反应也明显降低。发现以这种方式特异性抑制二次反应的能力相对持久,因为当二次攻击在诱导耐受后延迟长达4周时,大鼠的反应性降低。此外,在载体(SGG)耐受诱导之前对半抗原(TNP)进行致敏的大鼠,在用TNP-SGG攻击后,其抗TNP抗体也明显减少。这些发现表明,即使在载体特异性(SGG)辅助性细胞或半抗原特异性(TNP)B细胞致敏后,大鼠中也可诱导辅助性细胞耐受。这些结果与我们其他已发表的发现一致,即预先致敏大鼠中的IgE反应可被辅助性细胞耐受所克服。

相似文献

1
The induction of carrier-specific helper cell tolerance in presensitized rats.致敏大鼠中载体特异性辅助性T细胞耐受性的诱导。
Eur J Immunol. 1977 May;7(5):283-7. doi: 10.1002/eji.1830070508.
2
Effect of carrier-specific tolerance on the generation of helper cell function.载体特异性耐受对辅助细胞功能产生的影响。
Eur J Immunol. 1976 Oct;6(10):742-6. doi: 10.1002/eji.1830061016.
3
The effect of second signals on the induction of B cell tolerance: failure of helper T cells to block tolerance induction.第二信号对B细胞耐受性诱导的影响:辅助性T细胞无法阻断耐受性诱导。
Eur J Immunol. 1981 Jul;11(7):550-6. doi: 10.1002/eji.1830110706.
4
Hapten-specific T cell response to azobenzenearsonate-N-acetyl-L-tyrosine in the Lewis rat. II. Induction of helper activity demonstrated by TNP-haptenated ABA-peptide-Ficoll.Lewis大鼠对偶氮苯胂酸-N-乙酰-L-酪氨酸的半抗原特异性T细胞应答。II. 经TNP-半抗原化的ABA-肽-菲可诱导辅助活性的证明
J Immunol. 1983 Feb;130(2):579-85.
5
Functional differentiation of T cell precursors. I. Parameters of carrier-specific tolerance in murine helper T cell precursors.T细胞前体的功能分化。I. 小鼠辅助性T细胞前体中载体特异性耐受的参数。
J Immunol. 1979 Nov;123(5):2083-7.
6
Role of self carriers in the immune response and tolerance. VI. Induction and reversal of TNP-modified self unresponsiveness in vitro.自身载体在免疫应答和耐受中的作用。VI. 体外诱导和逆转经三硝基苯修饰的自身无反应性
J Immunol. 1980 Dec;125(6):2380-4.
7
Induction of antigen-specific antibody responses in primed and unprimed B cells. Functional heterogeneity among Th1 and Th2 T cell clones.在已致敏和未致敏的B细胞中诱导抗原特异性抗体反应。Th1和Th2 T细胞克隆之间的功能异质性。
J Immunol. 1989 Apr 15;142(8):2575-82.
8
The specificity of in vivo tolerance to haptens in NZB and normal mice after exposure to hapten-modified syngeneic spleen cells.在暴露于半抗原修饰的同基因脾细胞后,NZB小鼠和正常小鼠体内对半抗原的耐受性特异性。
J Immunol. 1982 Apr;128(4):1571-6.
9
Role of self-carriers in the immune response and tolerance. II. Parameters of tolerance induced by haptenated lymphoid cells.自身载体在免疫应答和耐受中的作用。II. 半抗原化淋巴细胞诱导的耐受参数。
Eur J Immunol. 1977 Jan;7(1):1-6. doi: 10.1002/eji.1830070102.
10
Two signals are required for accessory cells to induce B cell unresponsiveness. Tolerogenic Ig and prostaglandin.辅助细胞诱导B细胞无反应性需要两种信号。耐受性免疫球蛋白和前列腺素。
J Immunol. 1988 Jul 1;141(1):79-84.