<b>β</b>-mannosyl linkages inhibit CAWS arteritis by negatively regulating dectin-2-dependent signaling in spleen and dendritic cells

Hirata, Noriyuki; Ishibashi, Keiichiro; Sato, Wataru; Nagi-Miura, Noriko; Adachi, Yoshiyuki; Ohta, Shin; Ohno, Naohito

doi:10.3109/08923973.2013.830124

Cited by 12 publications

(12 citation statements)

References 41 publications

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“…4A to C). This result confirmed that sDectin-2-targeted liposome binding to the extracellular matrix was mannan specific, in agreement with the published carbohydrate specificity of sDectin-2 (42–46). We examined the stability of binding of DEC2-AmB-LLs to C.…”

Section: Resultssupporting

confidence: 91%

“…Dectin-2 is encoded by the human and mouse C-type LECtin receptor gene CLEC6A. Dectin-2 binds α-mannans and N-linked and O-linked mannans in mannoproteins (42–46). Dectin-2 is expressed in the plasma membrane of some lymphocytes, with its mannan binding domain (sDectin-2) on the outside of these cells and its signaling domain in the cytoplasm.…”

Section: Introductionmentioning

confidence: 99%

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Dectin-2-Targeted Antifungal Liposomes Exhibit Enhanced Efficacy

Ambati

Ellis

Lin

et al. 2019

mSphere

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Invasive fungal diseases caused by Candida albicans, Cryptococcus neoformans, and Aspergillus fumigatus have mortality rates ranging from 10 to 95%. Individual patient costs may exceed $100,000 in the United States. All antifungals in current use have serious limitations due to host toxicity and/or insufficient fungal cell killing that results in recurrent infections. Few new antifungal drugs have been introduced in the last 2 decades. Hence, there is a critical need for improved antifungal therapeutics. By targeting antifungal-loaded liposomes to α-mannans in the extracellular matrices secreted by these fungi, we dramatically reduced the effective dose of drug. Dectin-2-coated liposomes loaded with amphotericin B bound 50- to 150-fold more strongly to C. albicans, C. neoformans, and A. fumigatus than untargeted liposomes and killed these fungi more than an order of magnitude more efficiently. Targeting drug-loaded liposomes specifically to fungal cells has the potential to greatly enhance the efficacy of most antifungal drugs.

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Section: Resultssupporting

confidence: 91%

Section: Introductionmentioning

confidence: 99%

Dectin-2-Targeted Antifungal Liposomes Exhibit Enhanced Efficacy

Ambati

Ellis

Lin

et al. 2019

mSphere

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“…Unidentified RNA virus [25][26][27] Epstein-Barr virus 11,12) Candida albicans* 81) Human parvovirus B19 127) Human corona virus HCoV-NL63 121,122) Human vocavirus (HBoV) 125) Human immunodeficiency virus 124) Streptococcus pyrogenes 47) Staphyrococcus aureus 42,43) Yersinia pseudotuberculosis 76) Mycobacterium ssp 67) Lactobacillus casei* 130) α-mannan 87,132) β-glucan 128) Virus / Microbe dUTPase 15,123) TSST-1 35) SPEC 48) Possible effector molecule lipoarabinomannan 131) YPMa 64) Bacillus cereus 79) Candida ssp 72) A variant of Torque teno virus 7 126) Mycoplasma pneumoniae 129)…”

Section: Viruses Bacteria Fungiunclassified

“…KD-like vasculitis can be induced in rabbit, swine, and mouse models by various methods (80)(81)(82)(83). The known genetic background and ease of genetic manipulation have made mouse models the preferred model to investigate molecular pathogenesis of KD and to discover its therapeutic targets (84)(85)(86)(87)(88).…”

Section: Insight From Experimental Studies With Animal Model For Kdmentioning

confidence: 99%

Aetiological Significance of Infectious Stimuli in Kawasaki Disease

2019

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Kawasaki disease (KD) is a pediatric vasculitis syndrome that is often involves coronary artery lesions (e. g., coronary artery aneurysms). Although its causal factors and entire pathogenesis remain elusive, the available evidence indicates that the pathogenesis of KD is closely associated with dysregulation of immune responses to various viruses or microbes. In this short review, we address several essential aspects of the etiology of KD with respect to the immune response to infectious stimuli: 1) the role of viral infections, 2) the role of bacterial infections and the superantigen hypothesis, 3) involvement of innate immune response including pathogens/microbe-associated molecular patterns and complement pathways, and 4) the influence of genetic background on the response to infectious stimuli. Based on the clinical and experimental evidence, we discuss the possibility that a wide range of microbes and viruses could cause KD through common and distinct immune processes.

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“…This may explain why dectin-2 deficient mice are susceptible to C. albicans infection but, interestingly, not C. neoformans [148,149]. Dectin-2 may also detect -mannosyl linkages [150]. Dectin-2 can induce several cytokines and chemokines through multiple signalling pathways, including NF-B, MAPK, SYK, CARD9-Bcl10-Malt1, and PKC , and can activate the NLRP3 (NOD-like receptor family, pyrin domain containing 3) inflammasome and respiratory burst [87,151].…”

mentioning

confidence: 99%

CandidaImmunity

Naglik

2014

New Journal of Science

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The human pathogenic fungus Candida albicans is the predominant cause of both superficial and invasive forms of candidiasis. C. albicans primarily infects immunocompromised individuals as a result of either immunodeficiency or intervention therapy, which highlights the importance of host immune defences in preventing fungal infections. The host defence system utilises a vast communication network of cells, proteins, and chemical signals distributed in blood and tissues, which constitute innate and adaptive immunity. Over the last decade the identity of many key molecules mediating host defence against C. albicans has been identified. This review will discuss how the host recognises this fungus, the events induced by fungal cells, and the host innate and adaptive immune defences that ultimately resolve C. albicans infections during health.

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β-mannosyl linkages inhibit CAWS arteritis by negatively regulating dectin-2-dependent signaling in spleen and dendritic cells

Abstract: The α-mannosyl linkages of Candida mannan is a key molecule for the immunotoxicity. CAWS727, which conatins β-mannosyl linkages, competitively bound to lectin receptors, and resulted in reductions in the inflammatory response.

Cited by 12 publications

References 41 publications

Dectin-2-Targeted Antifungal Liposomes Exhibit Enhanced Efficacy

Dectin-2-Targeted Antifungal Liposomes Exhibit Enhanced Efficacy

Aetiological Significance of Infectious Stimuli in Kawasaki Disease

CandidaImmunity

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