Type II Collagen-induced Arthritis in Mice

Type II Collagen-induced Arthritis in Mice
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小鼠 II 型胶原诱导的关节炎

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通讯作者:
A. Kang
A. Kang
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作者:
J. Stuart;A. Townes;A. Kang

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Ⅱ型胶原在初次免疫后4 ~ 5周发生炎性关节炎。以完全相同的方式用变性II型胶原免疫对诱导关节炎无效。关节炎小鼠的细胞介导的免疫力通过测量在胶原存在下培养的单核细胞的[3 H]胸苷掺入来评估。免疫后2 wk,对胶原蛋白的增殖反应最强。当细胞与天然或变性的II型胶原或I型胶原一起培养时,发生同样良好的标记掺入。用变性胶原免疫的非关节炎小鼠的细胞反应与关节炎小鼠中观察到的细胞反应没有区别。通过ELISA测定胶原抗体来评估体液免疫。免疫后2 wk免疫球蛋白M(IgM)反应达高峰,5 wk免疫球蛋白IgG反应达高峰。用天然II型胶原免疫的关节炎小鼠的抗血清对天然II型分子上的构象决定簇是相对特异的,尽管注意到与变性胶原的一些反应性。用变性胶原免疫的非关节炎小鼠的抗血清主要识别共价结构决定簇。得出的结论是,天然II型胶原蛋白是必不可少的诱导关节炎和天然II型胶原蛋白特异性的抗体反应可能是重要的关节炎的发展。
type II collagen developed inflammatory arthritis between 4 and 5 wk after primary immunization. Immunization with denatured type II collagen in exactly the same manner was not effective in inducing arthritis. Cell-mediated immunity in arthritic mice was assessed by measuring [3H]thymidine incorporation by mononuclear cells cultured in the presence of collagen. The maximal proliferative response to collagen occurred at 2 wk after immunization. Equally good incorporation of label occurred when cells were cultured with native or denatured type II collagen or type I collagen. The cellular response of nonarthritic mice immunized with denatured collagen was indistinguishable from that seen in arthritic mice. Humoral immunity was assessed by an ELISA assay for antibodies to collagen. The immunoglobulin M (IgM) response peaked at 2 wk and the IgG response at 5 wk after immunization. Antisera from arthritic mice immunized with native type II collagen were relatively specific for conformational determinants on the native type II molecule although some reactivity with denatured collagen was noted. Antisera from nonarthritic mice immunized with denatured collagen primarily recognized covalent structural determinants. It was concluded that native type II collagen was essential for the induction of arthritis and that an antibody response specific for native type II collagen may be important for the development of arthritis.
DOI: 10.1002/art.1780270907
发表时间: 1984-01-01
影响因子: --
作者:
WOOLEY, PH;LUTHRA, HS;DAVID, CS
通讯作者: DAVID, CS