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Biozzi小鼠的胶原诱导性关节炎。关节受累与胶原II IgG2a自身抗体无关,也不仅限于H-2q和H-2r。

Collagen-induced arthritis in Biozzi mice. Joint involvement is not correlated with collagen II IgG2a autoantibodies nor restricted to only H-2q and H-2r.

作者信息

Bouvet J P, Couderc J, Bouthillier Y, Franc B, Decreusefond C, Mouton D

机构信息

Unité d'Immunologie Microbienne, Institut Pasteur, Paris, France.

出版信息

J Immunol. 1989 Sep 1;143(5):1537-42.

PMID:2760461
Abstract

High (H) and low (L) immune responder "Biozzi" mice, obtained by four different selections, were investigated for their ability to develop collagen-induced arthritis. Both LI and LII lines--characterized by their low antibody responses to a wide variety of Ag--developed arthritis though they do not bear the susceptible H-2q and H-2r haplotypes. Out of the two lines (HI and HII) selected for their high antibody responses and bearing H-2q, only one (HI) developed arthritis. Both the lines with amplified high or low antibody responses (HG and LG), and the lines differing in the levels of cell-mediated immunity (Hpha and Lpha), failed to develop arthritis. Collagen II autoantibodies were found in all the lines: the responses being high (HI and HG), low (LI, LII and LG), or intermediate (HII, Hpha and Lpha). The level of IgG2a autoantibodies, presumed to be the most pathogenic, was low in two (HI and LII) of the three arthritic lines, and was high in the unaffected HG line. These results show that this arthritis is not solely restricted to H-2q and H-2r haplotypes, and argue against a correlation between collagen autoantibody levels and disease incidence.

摘要

通过四种不同选择获得的高(H)和低(L)免疫应答“Biozzi”小鼠,对其发生胶原诱导性关节炎的能力进行了研究。LI和LII系——其特征是对多种抗原的抗体反应较低——尽管不携带易感的H-2q和H-2r单倍型,但仍发生了关节炎。在因高抗体反应而被选择且携带H-2q的两个品系(HI和HII)中,只有一个(HI)发生了关节炎。高或低抗体反应增强的两个品系(HG和LG)以及细胞介导免疫水平不同的品系(Hpha和Lpha)均未发生关节炎。在所有品系中均发现了II型胶原自身抗体:反应为高(HI和HG)、低(LI、LII和LG)或中等(HII、Hpha和Lpha)。在三个关节炎品系中的两个(HI和LII)中,被认为最具致病性的IgG2a自身抗体水平较低,而在未受影响的HG品系中则较高。这些结果表明,这种关节炎并不局限于H-2q和H-2r单倍型,并且反对胶原自身抗体水平与疾病发病率之间存在相关性。

相似文献

1
Collagen-induced arthritis in Biozzi mice. Joint involvement is not correlated with collagen II IgG2a autoantibodies nor restricted to only H-2q and H-2r.Biozzi小鼠的胶原诱导性关节炎。关节受累与胶原II IgG2a自身抗体无关,也不仅限于H-2q和H-2r。
J Immunol. 1989 Sep 1;143(5):1537-42.
2
Immunogenetics of type II collagen autoimmunity and susceptibility to collagen arthritis.II型胶原自身免疫的免疫遗传学与胶原性关节炎易感性
Immunology. 1988 Oct;65(2):305-10.
3
T helper subset involvement in two high antibody responder lines of mice (Biozzi mice): HI (susceptible) and HII (resistant) to collagen-induced arthritis.辅助性T细胞亚群参与两种对胶原诱导性关节炎有高抗体应答的小鼠品系(比奥齐小鼠):对胶原诱导性关节炎敏感的HI品系和抗性的HII品系。
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Type II collagen-induced arthritis in mice. IV. Variations in immunogenetic regulation provide evidence for multiple arthritogenic epitopes on the collagen molecule.小鼠Ⅱ型胶原诱导性关节炎。IV. 免疫遗传调控的变化为胶原分子上多个致关节炎表位提供了证据。
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Genetic susceptibility to murine collagen II autoimmune arthritis. Proposed relationship to the IgG2 autoantibody subclass response, complement C5, major histocompatibility complex (MHC) and non-MHC loci.小鼠胶原II型自身免疫性关节炎的遗传易感性。与IgG2自身抗体亚类反应、补体C5、主要组织相容性复合体(MHC)和非MHC基因座的潜在关系。
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Autoantibodies to murine type II collagen in collagen-induced arthritis: a comparison of susceptible and nonsusceptible strains.胶原诱导性关节炎中针对小鼠II型胶原的自身抗体:易感和非易感品系的比较
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Interactions between H-2 and background genes modulate collagen induced arthritis in high (HI) and low (LI) antibody producer Biozzi mice.H-2基因与背景基因之间的相互作用调节高抗体产生型(HI)和低抗体产生型(LI)Biozzi小鼠的胶原诱导性关节炎。
Immunol Lett. 1997 Jun;58(1):43-6. doi: 10.1016/s0165-2478(97)02708-9.
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Mls-1 and Mls-2 superantigens do not control susceptibility to collagen-induced arthritis in HI and HII mice.Mls-1和Mls-2超抗原并不控制HI和HII小鼠对胶原诱导性关节炎的易感性。
Immunology. 1993 Dec;80(4):661-3.

引用本文的文献

1
Mls-1 and Mls-2 superantigens do not control susceptibility to collagen-induced arthritis in HI and HII mice.Mls-1和Mls-2超抗原并不控制HI和HII小鼠对胶原诱导性关节炎的易感性。
Immunology. 1993 Dec;80(4):661-3.
2
Polymorphism of Tcrb and Tcrg genes in Biozzi mice: segregation analysis of a new Tcrg haplotype with antibody responsiveness.Biozzi小鼠中Tcrb和Tcrg基因的多态性:具有抗体反应性的新Tcrg单倍型的分离分析。
Immunogenetics. 1990;32(1):27-33. doi: 10.1007/BF01787325.
3
Expression of myosin-class II major histocompatibility complexes in the normal myocardium occurs before induction of autoimmune myocarditis.
肌球蛋白 II 类主要组织相容性复合体在正常心肌中的表达发生在自身免疫性心肌炎诱导之前。
Proc Natl Acad Sci U S A. 1992 Oct 1;89(19):9131-5. doi: 10.1073/pnas.89.19.9131.