CD36在树突状细胞功能调节中的作用。
A role for CD36 in the regulation of dendritic cell function.
作者信息
Urban B C, Willcox N, Roberts D J
机构信息
Weatherall Institute of Molecular Medicine, University of Oxford, John Radcliffe Hospital, Oxford OX3 9DS, United Kingdom.
出版信息
Proc Natl Acad Sci U S A. 2001 Jul 17;98(15):8750-5. doi: 10.1073/pnas.151028698. Epub 2001 Jul 10.
Dendritic cells (DC) are crucial for the induction of immune responses and thus an inviting target for modulation by pathogens. We have previously shown that Plasmodium falciparum-infected erythrocytes inhibit the maturation of DCs. Intact P. falciparum-infected erythrocytes can bind directly to CD36 and indirectly to CD51. It is striking that these receptors, at least in part, also mediate the phagocytosis of apoptotic cells. Here we show that antibodies against CD36 or CD51, as well as exposure to early apoptotic cells, profoundly modulate DC maturation and function in response to inflammatory signals. Although modulated DCs still secrete tumor necrosis factor-alpha, they fail to activate T cells and now secrete IL-10. We therefore propose that intact P. falciparum-infected erythrocytes and apoptotic cells engage similar pathways regulating DC function. These findings may have important consequences for the treatment of malaria and may suggest strategies for modulating pathological immune responses in autoimmune diseases.
树突状细胞（DC）对于免疫反应的诱导至关重要，因此是病原体进行调节的一个诱人靶点。我们之前已经表明，感染恶性疟原虫的红细胞会抑制DC的成熟。完整的感染恶性疟原虫的红细胞可以直接结合CD36，并间接结合CD51。引人注目的是，这些受体至少部分地也介导凋亡细胞的吞噬作用。在这里，我们表明，针对CD36或CD51的抗体，以及暴露于早期凋亡细胞，会深刻调节DC对炎症信号的成熟和功能。尽管被调节的DC仍然分泌肿瘤坏死因子-α，但它们无法激活T细胞，现在反而分泌白细胞介素-10。因此，我们提出完整的感染恶性疟原虫的红细胞和凋亡细胞参与了调节DC功能的相似途径。这些发现可能对疟疾的治疗具有重要意义，并且可能为调节自身免疫性疾病中的病理性免疫反应提供策略。
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