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本文引用的文献

1
Development of arthritis, periarthritis and periostitis in rats given adjuvants.给予佐剂的大鼠关节炎、关节周围炎和骨膜炎的发展。
Proc Soc Exp Biol Med. 1956 Jan;91(1):95-101. doi: 10.3181/00379727-91-22179.
2
Mapping and functional characterization of rat chromosome 4 regions that regulate arthritis models and phenotypes in congenic strains.调节同源近交系大鼠关节炎模型和表型的4号染色体区域的定位与功能特征分析。
Arthritis Rheum. 2003 Feb;48(2):551-9. doi: 10.1002/art.10782.
3
Positional identification of Ncf1 as a gene that regulates arthritis severity in rats.将Ncf1定位为调控大鼠关节炎严重程度的基因。
Nat Genet. 2003 Jan;33(1):25-32. doi: 10.1038/ng1058. Epub 2002 Dec 2.
4
Modulation of multiple experimental arthritis models by collagen-induced arthritis quantitative trait loci isolated in congenic rat lines: different effects of non-major histocompatibility complex quantitative trait loci in males and females.通过在同源近交系大鼠中分离出的胶原诱导性关节炎数量性状基因座对多种实验性关节炎模型进行调控：非主要组织相容性复合体数量性状基因座在雄性和雌性中的不同作用。
Arthritis Rheum. 2002 Aug;46(8):2225-34. doi: 10.1002/art.10439.
5
Arthritis induced in rats with nonimmunogenic adjuvants as models for rheumatoid arthritis.用非免疫原性佐剂在大鼠中诱导关节炎作为类风湿性关节炎的模型。
Immunol Rev. 2001 Dec;184:184-202. doi: 10.1034/j.1600-065x.2001.1840117.x.
6
Evaluation of quantitative trait loci regulating severity of mycobacterial adjuvant-induced arthritis in monocongenic and polycongenic rats: identification of a new regulatory locus on rat chromosome 10 and evidence of overlap with rheumatoid arthritis susceptibility loci.单基因和多基因大鼠中调节分枝杆菌佐剂诱导性关节炎严重程度的数量性状基因座评估：大鼠10号染色体上新调节基因座的鉴定以及与类风湿性关节炎易感基因座重叠的证据
Arthritis Rheum. 2002 Apr;46(4):1075-85. doi: 10.1002/art.10164.
7
Genetic links between the acute-phase response and arthritis development in rats.大鼠急性期反应与关节炎发展之间的遗传联系。
Arthritis Rheum. 2002 Jan;46(1):259-68. doi: 10.1002/1529-0131(200201)46:1<259::AID-ART10035>3.0.CO;2-2.
8
Map Manager QTX, cross-platform software for genetic mapping.Map Manager QTX，用于基因定位的跨平台软件。
Mamm Genome. 2001 Dec;12(12):930-2. doi: 10.1007/s00335-001-1016-3.
9
Cartilage-specific autoimmunity in rheumatoid arthritis: characterization of a triple helical B cell epitope in the integrin-binding-domain of collagen type II.类风湿关节炎中的软骨特异性自身免疫：II型胶原整合素结合域中一个三螺旋B细胞表位的特征
Eur J Immunol. 2001 Jun;31(6):1666-73. doi: 10.1002/1521-4141(200106)31:6<1666::aid-immu1666>3.0.co;2-t.
10
Rats made congenic for Oia3 on chromosome 10 become susceptible to squalene-induced arthritis.在10号染色体上针对Oia3基因构建近交系的大鼠，会变得易患角鲨烯诱导的关节炎。
Hum Mol Genet. 2001 Mar 15;10(6):565-72. doi: 10.1093/hmg/10.6.565.

胶原诱导性关节炎与 pristane 诱导性关节炎之间的比较基因分析。

A comparative genetic analysis between collagen-induced arthritis and pristane-induced arthritis.

作者信息

Olofsson Peter, Lu Shemin, Holmberg Jens, Song Tusheng, Wernhoff Patrik, Pettersson Ulf, Holmdahl Rikard

机构信息

Section for Medical Inflammation Research, Sölvegatan 19, I11 BMC, Lund University, S-22184 Lund, Sweden.

出版信息

Arthritis Rheum. 2003 Aug;48(8):2332-42. doi: 10.1002/art.11100.

DOI:10.1002/art.11100
PMID:12905489
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7159749/
Abstract

OBJECTIVE

To compare the genetic regulation of collagen-induced arthritis (CIA) with that of pristane-induced arthritis (PIA) in rats.

METHODS

A genome-wide linkage analysis of an (E3 x DA)DA backcross of rats with CIA (n = 364 male rats; the same strain combinations as previously used to determine the genetic control of PIA) was performed. The strongest loci in both CIA and PIA (i.e., Cia12/Pia4 and Cia13/Pia7) were isolated in congenic strains. Susceptibility in both congenic strains was tested in rats with CIA and in rats with PIA.

RESULTS

We found a striking, although not complete, similarity of the arthritis-controlling loci in CIA and in PIA, as well as the previously defined loci associated with cartilage destruction, antibody production, and the acute-phase response. All major PIA quantitative trait loci (QTLs) identified in early severe arthritis were also strong regulators of CIA. The 2 strongest QTLs, Cia12/Pia4 on chromosome 12 and Cia13/Pia7 on chromosome 4, were also analyzed in congenic strains with DA or E3 as the background genome. Consistent with the results of linkage analysis, the congenic strain experiments showed that the chromosome 4 locus was more penetrant in CIA than in PIA, while the chromosome 12 locus almost completely dominated the control of PIA severity.

CONCLUSION

The underlying genetic control of CIA was found to have many, but not all, pathogenic mechanisms in common with PIA, despite the use of a cartilage-specific antigen (type II collagen) to induce CIA but not PIA.

摘要

目的

比较大鼠胶原诱导性关节炎（CIA）与 pristane 诱导性关节炎（PIA）的基因调控。

方法

对患有 CIA 的大鼠（n = 364 只雄性大鼠；与先前用于确定 PIA 基因控制的相同品系组合）进行（E3×DA）DA 回交的全基因组连锁分析。在同源近交系中分离出 CIA 和 PIA 中最强的基因座（即 Cia12/Pia4 和 Cia13/Pia7）。在患有 CIA 和 PIA 的大鼠中测试这两种同源近交系的易感性。

结果

我们发现 CIA 和 PIA 中关节炎控制基因座存在显著但不完全相似之处，以及先前定义的与软骨破坏、抗体产生和急性期反应相关的基因座。在早期严重关节炎中鉴定出的所有主要 PIA 数量性状基因座（QTL）也是 CIA 的强调节因子。还在以 DA 或 E3 作为背景基因组的同源近交系中分析了 2 个最强的 QTL，即 12 号染色体上的 Cia12/Pia4 和 4 号染色体上的 Cia13/Pia7。与连锁分析结果一致，同源近交系实验表明，4 号染色体基因座在 CIA 中比在 PIA 中更具穿透性，而 12 号染色体基因座几乎完全主导了 PIA 严重程度的控制。

结论

尽管使用软骨特异性抗原（II 型胶原）诱导 CIA 而非 PIA，但发现 CIA 的潜在基因控制与 PIA 有许多（但并非全部）共同的致病机制。