系统性红斑狼疮中T细胞介导的抗DNA产生调节功能缺陷。
Deficiency of T cell mediated regulation of anti-DNA production in systemic lupus erythematosus.
作者信息
Clough J D, Frank S A, Calabrese L H
出版信息
Arthritis Rheum. 1980 Jan;23(1):24-9. doi: 10.1002/art.1780230105.
PMID:6965452
Abstract
Isolated B cells from normal subjects and patients with systemic lupus erythematosus (SLE) could be stimulated to produce IgM anti-DNA with pokeweed mitogen. Normal but not SLE allogeneic T cells abrogated this response. Normal but not SLE autologous T cells promoted a switch from IgM to IgG anti-DNA production. SLE is characterized by at least two types of immunoregulatory abnormalities: a defect in T suppressor function and a defect in the IgM to IgG switchover.
摘要
来自正常受试者和系统性红斑狼疮（SLE）患者的分离B细胞，可被美洲商陆丝裂原刺激产生IgM抗DNA。正常而非SLE的同种异体T细胞可消除这种反应。正常而非SLE的自体T细胞促进了从IgM抗DNA产生向IgG抗DNA产生的转换。SLE的特征在于至少两种免疫调节异常：T抑制功能缺陷和IgM向IgG转换缺陷。
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