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. 2023 Feb 9;13:2304. doi: 10.1038/s41598-023-29423-0

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© The Author(s) 2023

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

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CD36 mediated-effects on TLR signalling pathways in neonatal brain and immature human microglia. A diagram showing the mechanism of the scavenger receptor CD36-TLR mediated signalling in neonatal mouse brain as well as human microglia. (a) schematic representation of the methodology used. Neonatal mice and HMC3 cells were treated with LPS or anti-CD36 + LPS. (b) Upon activation by various ligands, the TLR2-CD36 mediated MyD88 dependent pathway activates transcription of various inflammatory cytokines. Activated endosomal TLR3 activates IRF3, which promotes transcription of the genes related to type 1 Interferons. Interestingly, IRF3 is also activated by TLR4, through the TRAM-TRIFF complex mediated cascade. (c) Blocking CD36 with the antibody prior to the LPS stimulation affects the TLR2 and TLR3 mediated signalling while the TLR4-IRF3 pathway continues to contribute to inflammation in both neonatal mouse as well as in human microglial cells. The schematic was created with BioRender.com.