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CD4或CD8缺陷小鼠的胶原诱导性关节炎:CD8 + T细胞在胶原诱导性关节炎的起始阶段起作用并调节其恢复阶段。

Collagen-induced arthritis in CD4- or CD8-deficient mice: CD8+ T cells play a role in initiation and regulate recovery phase of collagen-induced arthritis.

作者信息

Tada Y, Ho A, Koh D R, Mak T W

机构信息

Amgen Institute, Ontario Cancer Institute, Ontario, Canada.

出版信息

J Immunol. 1996 Jun 1;156(11):4520-6.

PMID:8666829
Abstract

Collagen-induced arthritis (CIA) is an experimental autoimmune disease induced by immunization with collagen type II (CII). We studied CIA in CD4- or CD8-deficient DBA/1 mice to further define the roles of CD4+ and CD8+ T cells in the disease. CD4-deficient mice developed severe arthritis, and no differences in incidence, clinical course, and severity were observed between CD4 -/- and CD4 +/- mice. Proliferative responses of lymph node T cells to CII was, however, reduced in CD4 -/- mice, and inflamed joints revealed relative accumulation of CD4-CD8-TCR(alpha)(beta)+ cells. A CII-specific T cell line generated from CD4-deficient mice responded to CII in a MHC-restricted fashion and had a CD4-CD8-TCR(alpha)(beta)+ phenotype. Disease incidence in CD8 -/- mice was significantly decreased compared with CD8 +/- mice, even though the severity of arthritis in arthritic mice was not different. These results suggests a role for CD8+ T cells in initiating CIA. Interestingly, CD8-deficient mice were more susceptible to a second induction of arthritis after remission of initial disease, pointing towards an immunoregulatory role for CD8+ T cells. CD8-deficient mice did not, however, show any defect in oral tolerance induction using CII. Taken together, our findings demonstrate that CD4-CD8-TCR(alpha)(beta) cells can trigger systemic arthritis in CD4-deficient mice and that CD8+ T cells can play dual and opposing roles, important both in initiation of CIA and in providing resistance to reinduction of CIA after recovery from initial disease.

摘要

胶原诱导性关节炎(CIA)是一种通过用II型胶原(CII)免疫诱导产生的实验性自身免疫性疾病。我们在CD4或CD8缺陷的DBA/1小鼠中研究了CIA,以进一步明确CD4+和CD8+T细胞在该疾病中的作用。CD4缺陷小鼠发生了严重的关节炎,在CD4 -/-和CD4 +/-小鼠之间未观察到发病率、临床病程和严重程度的差异。然而,CD4 -/-小鼠中淋巴结T细胞对CII的增殖反应降低,炎症关节显示CD4-CD8-TCR(α)(β)+细胞相对积聚。从CD4缺陷小鼠产生的CII特异性T细胞系以MHC限制性方式对CII作出反应,并具有CD4-CD8-TCR(α)(β)+表型。与CD8 +/-小鼠相比,CD8 -/-小鼠的疾病发病率显著降低,尽管关节炎小鼠的关节炎严重程度没有差异。这些结果表明CD8+T细胞在引发CIA中起作用。有趣的是,CD8缺陷小鼠在初始疾病缓解后对第二次关节炎诱导更敏感,这表明CD8+T细胞具有免疫调节作用。然而,CD8缺陷小鼠在使用CII诱导口服耐受方面未显示任何缺陷。综上所述,我们的研究结果表明,CD4-CD8-TCR(α)(β)细胞可在CD4缺陷小鼠中引发全身性关节炎,并且CD8+T细胞可发挥双重且相反的作用,这在CIA的起始以及从初始疾病恢复后对CIA再诱导的抵抗中均很重要。

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