C-Type Lectin-Like Receptors: Head or Tail in Cell Death Immunity

Drouin, Marion; Saenz, Javier; Chiffoleau, Elise

doi:10.3389/fimmu.2020.00251

Cited by 77 publications

(63 citation statements)

References 135 publications

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“…Densely glycosylated with multiple Asn-linked (N-glycans) and a few Ser/Thr-linked (O-glycans) 4 , 5 , the S protein of SARS-CoV-2 potentially presents ligands for a variety of innate immune receptors, including C-type lectin receptors (CLRs), that are known to bind specific glycans mostly in a Ca 2+ -dependent manner 6 , 7 . CLRs such as DC-SIGN/CD209, L-SIGN/CD209L/CLEC4M, mannose receptor/MR/MRC1/CD206, MGL/CLEC10A/CD301, and Dectin-2/CLEC6A, are highly expressed within the human immune system including monocytes, dendritic cells, and macrophages, functioning as the first-line of defense against invading viruses and pathogens 8 , 9 .…”

Section: Introductionmentioning

confidence: 99%

SARS-CoV-2 Spike Protein Interacts with Multiple Innate Immune Receptors

Gao

Zeng

Jia

et al. 2020

Preprint

109

147

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The spike (S) glycoprotein in the envelope of SARS-CoV-2 is densely glycosylated but the functions of its glycosylation are unknown. Here we demonstrate that S is recognized in a glycan-dependent manner by multiple innate immune receptors including the mannose receptor MR/CD206, DC-SIGN/CD209, L-SIGN/CD209L, and MGL/CLEC10A/CD301. Single-cell RNA sequencing analyses indicate that such receptors are highly expressed in innate immune cells in tissues susceptible to SARS-CoV-2 infection. Binding of the above receptors to S is characterized by affinities in the picomolar range and consistent with S glycosylation analysis demonstrating a variety of N- and O-glycans as receptor ligands. These results indicate multiple routes for SARS-CoV-2 to interact with human cells and suggest alternative strategies for therapeutic intervention.

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Section: Introductionmentioning

confidence: 99%

SARS-CoV-2 Spike Protein Interacts with Multiple Innate Immune Receptors

Gao

Zeng

Jia

et al. 2020

Preprint

109

147

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“…Interestingly, Mincle possesses a signal transduction pathway similar to the one from the osteoclast costimulators OSCAR (osteoclast associated, immunoglobulin-like receptor) and PIR-A (paired Ig-like receptor-A). It acts via the immunoreceptor tyrosine-based activation motif-harboring (ITAM-harboring) adaptor Fc receptor common γ subunit (FcRγ), leading to the activation of the spleen tyrosine kinase (SYK)/calcium axis (22,24). We therefore hypothesized that Mincle may represent the missing link between osteocyte death and osteoclast activation.…”

Section: Introductionmentioning

confidence: 99%

Osteocyte necrosis triggers osteoclast-mediated bone loss through macrophage-inducible C-type lectin

Andreev¹,

Liu²,

Weidner³

et al. 2020

Journal of Clinical Investigation

102

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“…After de ning histones as the main components of NETs to affect pericyte, we aimed to decipher the possible ways that pericyte might respond to. According to previous study, we converted our attention to C-type lectin receptors (CLRs), a large family of transmembrane receptors that recognized not only fungal moieties, but also histone-related molecules from dead cells [54,57]. Three types of CLRs are classi ed based on their molecular structures: type I, type II and soluble type.…”

Section: Resultsmentioning

confidence: 99%

Histones of Neutrophil Extracellular Traps (NETs) Activate Brain Pericyte via Dectin-1 in Traumatic Brain Injury

Liu

Zhang

et al. 2021

Preprint

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BackgroundBlood-brain barrier (BBB) disruption and leukocyte infiltration are two pathological features post traumatic brain injury (TBI). However, the role of circulating leukocytes in BBB disruption and the crosstalk between them are not fully elucidated. Neutrophil is the most abundant circulating cell type that migrates into brain tissue when TBI occurs instantly, while brain pericyte occupies a strategic position between circulating cell and interstitial space in BBB. Understanding their interactions is essential to provide insight into the intrinsic relationship and identify biological targets for TBI treatments. MethodsBy analyzing brain tissues from TBI patients and mouse TBI model through immunohistochemical method and flow cytometry, we build the relationship between neutrophils, neutrophil extracellular traps (NETs) and brain pericyte. The components of NETs-related medium were investigated by proteomics and metabolomics to decipher the factors directly regulating pericytes. The molecular mechanisms were deeply explored by WB/CHIP/RT-PCR in primary brain pericyte/pericyte cell line MBVP treated with NETs-formed medium or specific NETs components. In mice TBI model, we also explored the possible therapeutic approaches for TBI treatment that targeting at the axis of neutrophil-NETs-pericyte. ResultsNETs formation is highly enhanced post TBI, inducing the appearance of CD11b expressing brain pericyte simultaneously. This novel CD11b+ pericyte subset is characterized with increased permeability and pro-inflammatory profiles. Mechanistically, recognition of histones from NETs by Dectin-1 on pericyte contributes to CD11b induction in protein kinase C (PKC)-c-Jun-dependent manner. Transcription factor c-Jun directly binds to the promoter sequence of CD11b to enhance its expression in pericyte, conferring pericyte activation, BBB disruption and aggravated neutrophil infiltration post TBI. Either inhibiting NETs formation by Cl-Amidine or blocking Dectin-1 by Laminarin are both beneficial for decreasing neutrophil infiltration and brain pericyte activation post TBI. ConclusionsThese results unfold that “neutrophil-NETs-pericyte” and “histones-Dectin-1-CD11b” are possible cellular and molecular mechanisms for building connection between BBB damage and neutrophil infiltration. Targeting at NETs formation and Dectin-1 are promising treatments for improving neurological outcomes of TBI patients.

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C-Type Lectin-Like Receptors: Head or Tail in Cell Death Immunity

Cited by 77 publications

References 135 publications

SARS-CoV-2 Spike Protein Interacts with Multiple Innate Immune Receptors

SARS-CoV-2 Spike Protein Interacts with Multiple Innate Immune Receptors

Osteocyte necrosis triggers osteoclast-mediated bone loss through macrophage-inducible C-type lectin

Histones of Neutrophil Extracellular Traps (NETs) Activate Brain Pericyte via Dectin-1 in Traumatic Brain Injury

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