About: Dominant role of splenic marginal zone lipid rafts in the classical complement pathway against S. pneumoniae

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About: Dominant role of splenic marginal zone lipid rafts in the classical complement pathway against S. pneumoniae Goto Sponge NotDistinct Permalink

An Entity of Type : schema:ScholarlyArticle, within Data Space : wasabi.inria.fr associated with source document(s)

Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
title	Dominant role of splenic marginal zone lipid rafts in the classical complement pathway against S. pneumoniae
Creator	Choi, In-Soo Choi, Hyeongjwa Choi, Woo-Sung Jin, Yihwa Kang, Young-Sun Kim, Min-Kyung Park, Jin-Yeon Park, Min Lee, Yun Park, Seung Woo, Seung Yun, Tae Hwang, Han Joo, Jin
source	Medline; PMC
abstract	Lipid rafts (LRs) play crucial roles in complex physiological processes, modulating innate and acquired immune responses to pathogens. The transmembrane C-type lectins human dendritic cell-specific intercellular adhesion molecule-3-grabbing nonintegrin (DC-SIGN) and its mouse homolog SIGN-R1 are distributed in LRs and expressed on splenic marginal zone (MZ) macrophages. The DC-SIGN-C1q or SIGN-R1-C1q complex could mediate the immunoglobulin (Ig)-independent classical complement pathway against Streptococcus pneumoniae. Precise roles of LRs during this complement pathway are unknown. Here we show that LRs are indispensable for accelerating the DC-SIGN- or SIGN-R1-mediated classical complement pathway against S. pneumoniae, thus facilitating rapid clearance of the pathogen. The trimolecular complex of SIGN-R1-C1q-C4 was exclusively enriched in LRs of splenic MZ macrophages and their localization was essential for activating C3 catabolism and enhancing pneumococcal clearance, which were abolished in SIGN-R1-knockout mice. However, DC-SIGN replacement on splenic MZ macrophage’s LRs of SIGN-R1-depleted mice reversed these defects. Disruption of LRs dramatically reduced pneumococcal uptake and decomposition. Additionally, DC- SIGN, C1q, C4, and C3 were obviously distributed in splenic LRs of cadavers. Therefore, LRs on splenic SIGN-R1(+) or DC-SIGN(+) macrophages could provide spatially confined and optimal bidirectional platforms, not only for usual intracellular events, for example recognition and phagocytosis of pathogens, but also an unusual extracellular event such as the complement system. These findings improve our understanding of the orchestrated roles of the spleen, unraveling a new innate immune system initiated from splenic MZ LRs, and yielding answers to several long-standing problems, including the need to understand the profound role of LRs in innate immunity, the need to identify how such a small portion of splenic SIGN-R1(+) macrophages (<0.05% of splenic macrophages) effectively resist S. pneumoniae, and the need to understand how LRs can promote the protective function of DC-SIGN against S. pneumoniae in the human spleen.
has issue date	2019-09-09(xsd:dateTime)
bibo:doi	10.1038/s41420-019-0213-3
bibo:pmid	31531231
has license	cc-by
sha1sum (hex)	073d6557ccb048fe248c2d4c09a21c33f8632371
schema:url	https://doi.org/10.1038/s41420-019-0213-3
resource representing a document's title	Dominant role of splenic marginal zone lipid rafts in the classical complement pathway against S. pneumoniae
has PubMed Central identifier	PMC6733876
has PubMed identifier	31531231
schema:publication	Cell Death Discov
resource representing a document's body	covid:073d6557ccb048fe248c2d4c09a21c33f8632371#body_text
is schema:about of	named entity 'pathogens' named entity 'LRs' named entity 'However' named entity 'immunoglobulin' named entity 'Here' named entity 'splenic' named entity 'phagocytosis' covid:arg/073d6557ccb048fe248c2d4c09a21c33f8632371 named entity 'DC-SIGN' named entity 'expressed' named entity 'complex' named entity 'classical' named entity 'Therefore' named entity 'bidirectional' named entity 'classical' named entity 'innate' named entity 'complement pathway' named entity 'LRs' named entity 'macrophages' named entity 'C-type' named entity 'platforms' named entity 'innate immune system' named entity 'human' named entity 'marginal zone' named entity 'DC-SIGN' named entity 'macrophages' named entity 'complement pathway' named entity 'physiological processes' named entity 'C-type lectins' named entity 'immunoglobulin' named entity 'Lipid rafts' named entity 'spleen' named entity 'catabolism' named entity 'phagocytosis' named entity 'spleen' named entity 'lipid rafts' named entity 'splenic' named entity 'marginal zone' named entity 'S. pneumoniae' named entity 'organism' named entity 'Staphylococcus aureus' named entity 'Millipore' named entity '0.01' named entity 'infection' named entity 'Splenic' named entity 'macrophages' named entity 'complement activation' named entity 'DC-SIGN' named entity 'DC-SIGN' named entity 'spleen' named entity 'FACS' named entity 'fluorescent' named entity '2-phenylindole' named entity 'CD55' named entity 'phagocytosis' named entity 'homolog' named entity '37°C' named entity 'DC-SIGN' named entity 'S. pneumoniae' named entity 'C1q' named entity 'pneumococcal' named entity 'gradient' named entity 'statistical significance' named entity 'S. pneumoniae' named entity 'dynamin' named entity 'San Jose' named entity 'IgG' named entity 'iC3b'

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