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Cited by 318

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A role for CD36 in the regulation of dendritic cell function

Open access
Urban, Britta C., Willcox, Nick, Roberts, David J.·2001·Proceedings of the National Academy of Sciences

Abstract

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-α, 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.

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Metadata

Authors
Urban, B. C., Willcox, N., & Roberts, D. J.
Venue
Proceedings of the National Academy of Sciences
Published
2001-07-10
Volume
98
Issue
15
Pages
8750-8755
ISSN
  • 0027-8424 (ISSN-L)
  • 1091-6490
OpenAlex
W2043418529
Cited by
318
References
1
FWCI
7.13
Type
journal article
Language
en
Open access
green

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CoChat. (2026). Citation check: A role for CD36 in the regulation of dendritic cell function. https://app.cochat.ai/papers/10.1073/pnas.151028698
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Urban, B. C., Willcox, N., & Roberts, D. J. (2001). A role for CD36 in the regulation of dendritic cell function. Proceedings of the National Academy of Sciences. https://doi.org/10.1073/pnas.151028698

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

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