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. 2023 Aug 14;14:4895. doi: 10.1038/s41467-023-40635-w

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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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Fig. 7 — TLR4 modulates the surface expression of MSR1 through a yet-to-be-identified mechanism, such that loss of TLR4 signalling drives increased surface expression of MSR1. This may be through modulation of MSR1 gene expression or modulation of intracellular MSR1 reservoir trafficking to the plasma membrane. MSR1 is then responsible for the direct binding and internalisation of C. neoformans. MSR1-mediated uptake may rely on the formation of a signalling complex with FcγRII/III. The ITAM domain of FcγRs enables SYK and PI3K activation which then activates Rac GTPases that drive actin polymerisation and phagocytosis. At the same time, TLR3, MyD88 and TRIF may also serve as coreceptors or adaptor proteins leading to the activation of ERK1/2 and p38 which will also drive actin remodelling and pathogen uptake. Figure created with BioRender.com.