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来自胶原诱导性关节炎小鼠的CD4 + T细胞对于将关节炎转移至严重联合免疫缺陷小鼠至关重要。

CD4+ T cells from collagen-induced arthritic mice are essential to transfer arthritis into severe combined immunodeficient mice.

作者信息

Kadowaki K M, Matsuno H, Tsuji H, Tunru I

机构信息

Department of Orthopaedic Surgery, Toyama Medical and Pharmaceutical University, Japan.

出版信息

Clin Exp Immunol. 1994 Aug;97(2):212-8. doi: 10.1111/j.1365-2249.1994.tb06070.x.

Abstract

The role of T lymphocytes in the adoptive transfer of collagen-induced arthritis (CIA) in DBA/1J mice to severe combined immunodeficient (SCID) mice was investigated. Spleen cells from non-immunized, type I collagen (CI) or type II collagen (CII)-immunized DBA/1J mice were injected into SCID mice which lack functional T and B cells. Specific antigenic stimulation of arthritogenic cells was required since only lymphocytes from arthritic CIA mice plus simultaneous administration of CII transferred arthritis to 11 of 12 SCID mice with a marked increase in CII antibody titre. However, CI-immunized or non-immunized DBA/1J mice cells did not induce arthritis in SCID mice. SCID recipients of pre-arthritic CIA lymphocytes presented increase in CII antibody, but showed no clinical signs of arthritis, suggesting that antibodies to CII alone can not induce CIA. Depletion of CD4+ T cells inhibited the transfer of arthritis to SCID mice, with a decrease in CII antibody titre in chimaeras. In contrast, depletion of CD8+ T cells enhanced the onset of arthritis in SCID mice. The results imply that CD4+ T cells are required for the induction of CIA. In addition, CD8+ T cells might have a suppressive role in the etiology of this disease. It is probable that memory CD4+ T cells stimulate production of antibodies to CII and subsequent arthritis. This study clarifies the role of T lymphocytes in the transfer of CIA to SCID mice.

摘要

研究了T淋巴细胞在将DBA/1J小鼠胶原诱导性关节炎(CIA)过继转移至重症联合免疫缺陷(SCID)小鼠中的作用。将来自未免疫、I型胶原(CI)或II型胶原(CII)免疫的DBA/1J小鼠的脾细胞注射到缺乏功能性T细胞和B细胞的SCID小鼠体内。致关节炎细胞的特异性抗原刺激是必需的,因为只有来自关节炎性CIA小鼠的淋巴细胞加上同时给予CII才能将关节炎转移至12只SCID小鼠中的11只,且CII抗体滴度显著升高。然而,CI免疫或未免疫的DBA/1J小鼠细胞未在SCID小鼠中诱导出关节炎。关节炎前期CIA淋巴细胞的SCID受体CII抗体增加,但未表现出关节炎的临床症状,这表明单独针对CII的抗体不能诱导CIA。CD4+ T细胞的耗竭抑制了关节炎向SCID小鼠的转移,嵌合体中CII抗体滴度降低。相反,CD8+ T细胞的耗竭增强了SCID小鼠中关节炎的发作。结果表明,CD4+ T细胞是诱导CIA所必需的。此外,CD8+ T细胞可能在该疾病的病因中具有抑制作用。记忆性CD4+ T细胞可能刺激产生针对CII的抗体并随后引发关节炎。本研究阐明了T淋巴细胞在将CIA转移至SCID小鼠中的作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d216/1534708/d1b8513f4a9e/clinexpimmunol00028-0046-a.jpg

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