CLEC5A is critical for dengue virus-induced osteoclast activation and bone homeostasis

Huang, Ya Lang; Chen, Szu Ting; Liu, Ru‐Shi; Chen, Yen Hsu; Lin, Chun Yu; Huang, Chung Hao; Shu, Pei-Yun; Liao, Ching Len; Hsieh, Shie Liang

doi:10.1007/s00109-016-1409-0

Cited by 33 publications

(23 citation statements)

References 33 publications

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“…Osteoclasts are multinucleated giant cells that differentiate from macrophages and are involved in bone remodeling [116]. DV infection of osteoclasts was recently shown to upregulate osteolytic activity [117]. Attenuation of DV-induced osteolytic activity was observed in MDL-1 -/- mice and, consistently, administration of a MDL-1 antagonist in wild-type mice also inhibited DV-activated osteolytic activity [117].…”

Section: Myeloid C-type Lectins Receptors—pattern Recognition Recementioning

confidence: 99%

Myeloid C-Type Lectin Receptors in Viral Recognition and Antiviral Immunity

Monteiro

Lepenies

2017

Viruses

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Recognition of viral glycans by pattern recognition receptors (PRRs) in innate immunity contributes to antiviral immune responses. C-type lectin receptors (CLRs) are PRRs capable of sensing glycans present in viral pathogens to activate antiviral immune responses such as phagocytosis, antigen processing and presentation, and subsequent T cell activation. The ability of CLRs to elicit and shape adaptive immunity plays a critical role in the inhibition of viral spread within the host. However, certain viruses exploit CLRs for viral entry into host cells to avoid immune recognition. To block CLR interactions with viral glycoproteins, antiviral strategies may involve the use of multivalent glycan carrier systems. In this review, we describe the role of CLRs in antiviral immunity and we highlight their dual function in viral clearance and exploitation by viral pathogens.

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Section: Myeloid C-type Lectins Receptors—pattern Recognition Recementioning

confidence: 99%

Myeloid C-Type Lectin Receptors in Viral Recognition and Antiviral Immunity

Monteiro

Lepenies

2017

Viruses

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“…Moreover, dengue virus activates the NLRP3 inflammasome via CLEC5A to induce the production of IL-1β and IL-18 6 , 7 . We have previously shown that dengue virus activates CLEC5A to upregulate osteolytic activity and dysregulate bone homeostasis 8 . Blockade of CLEC5A by anti-CLEC5A monoclonal antibody (mAb) not only attenuates dengue virus-induced and Japanese encephalitis virus-induced lethality, but also suppresses dengue virus-mediated activation of the NLRP3 inflammasome and osteolytic activity 4 , 8 .…”

Section: Introductionmentioning

confidence: 99%

“…We have previously shown that dengue virus activates CLEC5A to upregulate osteolytic activity and dysregulate bone homeostasis 8 . Blockade of CLEC5A by anti-CLEC5A monoclonal antibody (mAb) not only attenuates dengue virus-induced and Japanese encephalitis virus-induced lethality, but also suppresses dengue virus-mediated activation of the NLRP3 inflammasome and osteolytic activity 4 , 8 . These findings suggest that CLEC5A has critical functions in flavivirus-induced inflammatory reactions.…”

Section: Introductionmentioning

confidence: 99%

CLEC5A is a critical receptor in innate immunity against Listeria infection

Chen

Hsu

et al. 2017

Nat Commun

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The C-type lectin member 5A (CLEC5A) is a pattern recognition receptor for members of the Flavivirus family and has critical functions in response to dengue virus and Japanese encephalitis virus. Here we show that CLEC5A is involved in neutrophil extracellular trap formation and the production of reactive oxygen species and proinflammatory cytokines in response to Listeria monocytogenes. Inoculation of Clec5a −/− mice with L. monocytogenes causes rapid bacterial spreading, increased bacterial loads in the blood and liver, and severe liver necrosis. In these mice, IL-1β, IL-17A, and TNF expression is inhibited, CCL2 is induced, and large numbers of CD11b+Ly6ChiCCR2hiCX3CR1low inflammatory monocytes infiltrate the liver. By day 5 of infection, these mice also have fewer IL-17A+ γδ T cells, severe liver necrosis and a higher chance of fatality. Thus, CLEC5A has a pivotal function in the activation of multiple aspects of innate immunity against bacterial invasion.

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“…Members of C-type lectins have been shown to be crucial pattern recognition receptors that recognize members of the flavivirus and influenza virus families. Spleen tyrosine kinase (Syk)–coupled C-type lectin member 5A (CLEC5A) is the pattern recognition receptor (PRR) for the dengue virus (DV) 14 – 16 , Japanese encephalitis virus (JEV) 17 , and influenza virus H5N1 18 . These viruses can activate CLEC5A to secrete abundant proinflammatory cytokines from macrophages and myeloid cells; blockade of CLEC5A can protect mice from DV- and JEV-induced lethality and neuroinflammation.…”

Section: Introductionmentioning

confidence: 99%

Association of C-type lectin 18 levels with extrahepatic manifestations in chronic HCV infection

Liao

Huang

Chen

et al. 2018

Sci Rep

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Mixed cryobulinemia (MC) is the most common chronic hepatitis C virus (HCV)-associated extrahepatic manifestation. C-type lectin 18 (CLEC18) is a novel secretory lectin that is abundantly expressed in hepatocytes and peripheral blood cells (PBCs). We investigated the associations between CLEC18 expression during HCV infection and the presence of extrahepatic manifestations. A total of 41 rheumatic patients with HCV infection (including 28 patients with MC syndrome), 45 rheumatic patients without infection, and 14 healthy subjects were enrolled. The CLEC18 levels in PBCs and serum were determined by using flow cytometry and enzyme-linked immunosorbent assay, respectively. Significantly higher CLEC18 levels were observed in patients with HCV infection (P < 0.001) and were positively correlated with HCV viral loads (γ = 0.56, P < 0.05). Among patients with HCV infection, significantly increased CLEC18 levels were observed in patients with MC syndrome, particularly in those with type II MC (P < 0.05). CLEC18 levels were associated with cryoglobulin and C4 levels (P < 0.05). CLEC18 was significantly associated with HCV infection, particularly in those with HCV-associated MC. CLEC18 levels were also positively correlated with MC disease activity, suggesting its involvement in MC pathogenesis. CLEC18 may be a novel indicator of HCV infection and a potential therapeutic target in rheumatic patients.

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CLEC5A is critical for dengue virus-induced osteoclast activation and bone homeostasis

Cited by 33 publications

References 33 publications

Myeloid C-Type Lectin Receptors in Viral Recognition and Antiviral Immunity

Myeloid C-Type Lectin Receptors in Viral Recognition and Antiviral Immunity

CLEC5A is a critical receptor in innate immunity against Listeria infection

Association of C-type lectin 18 levels with extrahepatic manifestations in chronic HCV infection

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