{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Yang SW"],"funding":["Korea Health Industry Development Institute","National Research Foundation of Korea"],"pagination":["133"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC6733876"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["5"],"pubmed_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 <i>Streptococcus pneumoniae</i>. 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 <i>S. pneumoniae</i>, thus facilitating rapid clearance of the pathogen. The"],"journal":["Cell death discovery"],"pubmed_title":["Dominant role of splenic marginal zone lipid rafts in the classical complement pathway against <i>S. pneumoniae</i>."],"pmcid":["PMC6733876"],"funding_grant_id":["S201803S00049","HI17C1713","NRF2017R1C1B2010487"],"pubmed_authors":["Choi H","Yun TJ","Park M","Lee YK","Joo JS","Jin Y","Yang SW","Choi IS","Park JY","Choi WS","Kim MK","Park SH","Hwang HS","Kang YS"],"additional_accession":[]},"is_claimable":false,"name":"Dominant role of splenic marginal zone lipid rafts in the classical complement pathway against <i>S. pneumoniae</i>.","description":"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 <i>Streptococcus pneumoniae</i>. 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 <i>S. pneumoniae</i>, thus facilitating rapid clearance of the pathogen. The","dates":{"release":"2019-01-01T00:00:00Z","publication":"2019","modification":"2025-04-04T08:29:48.402Z","creation":"2019-09-24T07:09:10Z"},"accession":"S-EPMC6733876","cross_references":{"pubmed":["31531231"],"doi":["10.1038/s41420-019-0213-3"]}}