About: MBL Deficiency as Risk of Infection and Autoimmunity

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

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type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
title	MBL Deficiency as Risk of Infection and Autoimmunity
Creator	Gupta, Anita
source	PMC
abstract	In pathogen recognition by C-type lectins, several levels of complexity can be distinguished; these might modulate the immune response in different ways. Firstly, the pathogen-associated molecular pattern repertoire expressed at the microbial surface determines the interactions with specific receptors (Fig. 42.1). Secondly, each immune cell type possesses a specific set of pathogen-recognition receptors. Thirdly, changes in the cell-surface distribution of C-type lectins regulate carbohydrate binding by modulating receptor affinity for different ligands. Crosstalk between these receptors results in a network of multimolecular complexes, adding a further level of complexity in pathogen recognition (Cambi and Figdor 2005; Thiel et al. 2006) (see 10.1007/978-3-7091-1065-2_23). MBL deficiency is genetically determined and predisposes to recurrent infections and chronic inflammatory diseases. MBL deficiency has been implicated in susceptibility and course of viral, bacterial, fungal, and protozoan infection. More than 10% of the general population may, depending on definition, be classified as MBL deficient, underlining the redundancy of the immune system. MBL-disease association studies have been a fruitful area of research, which implicates a role for MBL in infective, inflammatory and autoimmune disease processes. MBL deficiency predisposes both to infection by extra-cellular pathogens and to autoimmune disease.
has issue date	2012-03-20(xsd:dateTime)
bibo:doi	10.1007/978-3-7091-1065-2_42
has license	no-cc
sha1sum (hex)	b945ada94a3cdf6f7a5f828647e616dc7e1d76b7
schema:url	https://doi.org/10.1007/978-3-7091-1065-2_42
resource representing a document's title	MBL Deficiency as Risk of Infection and Autoimmunity
has PubMed Central identifier	PMC7122001
schema:publication	Animal Lectins: Form, Function and Clinical Applications
resource representing a document's body	covid:b945ada94a3cdf6f7a5f828647e616dc7e1d76b7#body_text
is schema:about of	named entity 'MBL DEFICIENCY' named entity 'AUTOIMMUNITY' named entity 'RISK OF INFECTION' named entity 'malignant disease' named entity 'immunogenetic' named entity 'molecule' named entity 'SLE' named entity 'SNPs' named entity 'peripheral nerve damage' named entity 'serum' named entity 'heart failure' named entity 'lupus nephritis' named entity 'kDa' named entity 'apoptotic cells' named entity 'alleles' named entity 'protozoa' named entity 'cell lines' named entity 'genotyping' named entity 'autologous' named entity 'immune complexes' named entity 'gliadin' named entity 'HCV' named entity 'serum levels' named entity 'cell lines' named entity 'autoimmunity' named entity 'rheumatic disorders' named entity 'haplotypes' named entity 'MBL deficiency' named entity 'MBP deficiency' named entity 'MBL deficiency' named entity 'protein' named entity 'ischemia/reperfusion' named entity 'cross-reactive' named entity 'keratinocytes' named entity 'respiratory tract infections' named entity 'albuminuria' named entity 'ligands' named entity 'HIV' named entity 'exon' named entity 'DKO' named entity 'MBL2' named entity 'virus' named entity 'AMI' named entity 'oncogenic transformation' named entity 'genotypes' named entity 'environmental factors' named entity 'infection' named entity 'chronic gastritis' named entity 'hemopoietic' named entity 'cardiovascular complications' named entity 'genetic factors' named entity 'mutation' named entity 'haplotype' named entity 'diabetic nephropathy' named entity 'allele' named entity 'mutation' named entity 'antigens' named entity 'cell surface' named entity 'apoptotic cells' named entity 'rheumatoid arthritis' named entity 'polymorphism' named entity 'multivalent' named entity 'C. albicans' named entity 'mannose' named entity 'SLE' named entity 'anti-double stranded DNA' named entity 'complement pathway' named entity 'allele' named entity 'SLE' named entity 'infectious disease' named entity 'alleles' named entity 'membranous nephropathy' named entity 'cecal' named entity 'SARS' named entity 'MBL deficiency' named entity 'rheumatoid arthritis' named entity 'genotypes' named entity 'infection' named entity 'cystic fibrosis' named entity 'SNPs' named entity 'auto-antibodies' named entity 'haplotypes' named entity 'homozygous'

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