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大鼠胶原诱导性关节炎和佐剂诱导性关节炎。用胶原进行免疫后治疗以抑制或消除关节炎反应。

Collagen-induced and adjuvant-induced arthritis in rats. Post-immunization treatment with collagen to suppress or abrogate the arthritic response.

作者信息

Phadke K, Fouts R, Parrish J E

出版信息

Arthritis Rheum. 1984 Jul;27(7):797-806. doi: 10.1002/art.1780270711.

Abstract

Immunization of Lewis rats with native type II collagen results in an inflammatory arthritis and increased humoral and cellular immune responses to type II collagen. The exposure of rats to native type II collagen at day 7 or 10 after immunization suppressed the incidence of arthritis and anticollagen antibody levels, although the cellular response was not affected. The exposure to denatured type II collagen offered partial protection, while type I collagen had no significant effect. Rats immunized with Mycobacterium tuberculosis also showed reduced arthritic response when subsequently treated with type II collagen. The common modalities between the 2 models and the possible role of type II collagen in the interference with the inflammatory arthritic events are discussed.

摘要

用天然II型胶原免疫Lewis大鼠可导致炎症性关节炎,并增强对II型胶原的体液免疫和细胞免疫反应。在免疫后第7天或第10天将大鼠暴露于天然II型胶原,可抑制关节炎的发病率和抗胶原抗体水平,尽管细胞反应未受影响。暴露于变性II型胶原可提供部分保护,而I型胶原则无显著作用。用结核分枝杆菌免疫的大鼠在随后用II型胶原治疗时,关节炎反应也会降低。本文讨论了这两种模型之间的共同模式以及II型胶原在干扰炎症性关节炎事件中的可能作用。

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