Antigen presentation by renal tubular epithelial cells.
Antigen presentation by renal tubular epithelial cells.
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发表时间：
1991-07
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通讯作者：
V. Rubin‐Kelley;A. Jevnikar
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作者：
V. Rubin‐Kelley;A. Jevnikar
在器官特异性免疫损伤中，免疫效应细胞如T淋巴细胞和实质细胞之间的相互作用是动态的。现在可以理解，这种相互作用的特异性、强度和最终的破坏性影响可以受到目标问题的响应的极大影响。肾小管细胞特别适合参与这种免疫协作。(1)它们暴露于来自血液和肾小球滤液的无数潜在免疫原性肽，并且具有进一步加工这些肽的途径;（2）它们表达促进它们与T细胞接合的表面分子;以及（3）它们可以产生促炎细胞因子。在目前研究的免疫介导的肾小管间质损伤模型中，人们对确定启动、加速或抑制疾病的T淋巴细胞有很大的兴趣。令人惊讶的是，已经有相对较少的关注定义的肾小管细胞反应，调节这些免疫介导的过程。因此，这篇综述将集中在免疫肾小管损伤的这一有趣的方面，并涉及已知的自身免疫性肾病中肾小管细胞的抗原呈递。
The interaction between immune effector cells such as T lymphocytes and parenchymal cells in organ-specific immune injury is dynamic. It is now appreciated that the specificity, intensity, and eventual destructive effects of such interactions can be greatly influenced by responses of the target issue. Renal tubular cells are particularly well suited to participate in such immune collaborations. (1) They are exposed to innumerable potentially immunogenic peptides from blood and glomerular filtrate and have pathways to further process these peptides; (2) they express surface molecules which facilitate their engagement to T cells; and (3) they can produce proinflammatory cytokines. In the models of immune-mediated tubulointerstitial injury that are currently studied, there has been a great interest in defining the T lymphocytes that initiate, accelerate, or suppress disease. Surprisingly, there has been relatively little attention on defining the tubular cell responses that regulate these immune-mediated processes. This review will therefore focus on this intriguing aspect of immune tubular injury and relate what is known about antigen presentation by tubular cells in autoimmune renal disease.