The pathology of T cells in systemic lupus erythematosus.
The pathology of T cells in systemic lupus erythematosus.
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全身性红斑狼疮中T细胞的病理。
DOI：
10.1155/2014/419029
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发表时间：
2014
影响因子：
4.1
通讯作者：
Kow NY
中科院分区：
文献类型：
--
作者：
Mak A;Kow NY
系统性红斑狼疮（SLE）的特点是产生广泛的自身抗体。因此，该病症传统上被归类为“B细胞疾病”。然而，令人信服的证据表明，如果没有辅助性T淋巴细胞的帮助，“无助的”B细胞确实很难变得有足够的功能来触发SLE相关的炎症。已经认识到T细胞通过其与B细胞通信并提供巨大帮助以驱动自身抗体产生的能力在SLE的致病性中是至关重要的。最近，已经在狼疮T细胞中鉴定了许多增加触发狼疮相关炎症的倾向的表型和功能改变。在这里，涉及T细胞受体表达，受体后下游信号转导，表观遗传学和氧化应激，有利于激活狼疮T细胞的改变的潜在机制将进行讨论。此外，调节性CD4+、CD8+和γδ T细胞如何调节狼疮相关炎症将被强调。最后，虽然目前可用的临床试验评估的治疗药物，操纵T细胞，如钙调磷酸酶抑制剂的结果表明，他们至少是有效的和安全的常规免疫抑制剂在治疗狼疮肾小球肾炎，更大的临床试验无疑需要验证这些尚未有利的发现。
Systemic lupus erythematosus (SLE) is characterized by the production of a wide array of autoantibodies. Thus, the condition was traditionally classified as a “B-cell disease”. Compelling evidence has however shown that without the assistance of the helper T lymphocytes, it is indeed difficult for the “helpless” B cells to become functional enough to trigger SLE-related inflammation. T cells have been recognized to be crucial in the pathogenicity of SLE through their capabilities to communicate with and offer enormous help to B cells for driving autoantibody production. Recently, a number of phenotypic and functional alterations which increase the propensity to trigger lupus-related inflammation have been identified in lupus T cells. Here, potential mechanisms involving alterations in T-cell receptor expressions, postreceptor downstream signalling, epigenetics, and oxidative stress which favour activation of lupus T cells will be discussed. Additionally, how regulatory CD4+, CD8+, and γδ T cells tune down lupus-related inflammation will be highlighted. Lastly, while currently available outcomes of clinical trials evaluating therapeutic agents which manipulate the T cells such as calcineurin inhibitors indicate that they are at least as efficacious and safe as conventional immunosuppressants in treating lupus glomerulonephritis, larger clinical trials are undoubtedly required to validate these as-yet favourable findings.