Mostrar el registro sencillo del ítem

The role of nuclear factors as “Find-Me”/alarmin signals and immunostimulation in defective efferocytosis and related disorders

dc.contributor.authorTajbakhsh A.
dc.contributor.authorRezaee M.
dc.contributor.authorBarreto G.E.
dc.contributor.authorMoallem S.A.
dc.contributor.authorHenney N.C.
dc.contributor.authorSahebkar A.
dc.date.accessioned2020-09-02T22:29:23Z
dc.date.available2020-09-02T22:29:23Z
dc.date.issued2020
dc.identifier10.1016/j.intimp.2019.106134
dc.identifier.citation80, , -
dc.identifier.issn15675769
dc.identifier.urihttps://hdl.handle.net/20.500.12728/6437
dc.descriptionEfferocytosis as an apoptotic cell (AC) clearance mechanism facilitates the removal of dangerous and damaged cells, an important process in regulating normal homeostasis. Failure to correctly execute apoptosis and efferocytosis is associated with atherosclerosis, as well as chronic inflammatory and autoimmune disorders such as systemic lupus erythematosus (SLE). Effective and timely efferocytosis involves various molecules that act as “Find-Me” signals or as alarmins to quickly allow identification by phagocytic cells. In recent years, most of these molecules have been investigated, but less attention has been paid to the nuclear molecules associated with efferocytosis of ACs and necrotic cells (NCs). These molecules have several functions including acting as alarmin signals for faster recognition of ACs, facilitating the cleanup of ACs and for maintaining self-tolerance. The same group of molecules is also implicated in several inflammatory and autoimmune diseases. Previous studies have shown that these molecules also serve as targets for pharmacological agents such as necrostatins, recombinant Fcnb, anti-histone, neutralizing antibodies, calbiochem, aminophylline, activated protein C, CD24IgG recombinant fission protein, and recombinant thrombomodulin. Thus, greater understanding of these molecules/pathways will enable developments in the treatment and/or prevention of various disorders, especially autoimmune diseases. Here, we review current knowledge about the mechanisms by which nucleic acids, histones, nucleosomes and monosodium urate microcrystals (MSU) can act as alarmins/“Find-Me” signals, how they might be stimulated in defective efferocytosis and their function and importance as biomarkers for prognosis and treatment of atherosclerosis, inflammatory disorders and autoimmune diseases. © 2020 Elsevier B.V.
dc.language.isoen
dc.publisherElsevier B.V.
dc.subjectAuto-antigen
dc.subjectChromatin
dc.subjectDAMPs
dc.subjectFree DNA
dc.subjectImmune tolerance
dc.subjectMacrophage clearances
dc.subjectPhagocytosis
dc.subjectSelf-nucleic acid
dc.subjectadvanced glycation end product receptor
dc.subjectCD24 antigen
dc.subjectcomplement component C1q
dc.subjectdeoxyribonuclease
dc.subjecthigh mobility group B1 protein
dc.subjecthistone
dc.subjecthistone deacetylase
dc.subjectnuclear factor
dc.subjectnucleic acid
dc.subjectserum amyloid P
dc.subjecttoll like receptor
dc.subjecturate
dc.subjectapoptosis
dc.subjectatherosclerosis
dc.subjectautoimmune disease
dc.subjectcrystal
dc.subjectDNA RNA hybridization
dc.subjectefferocytosis
dc.subjecthuman
dc.subjectimmunological tolerance
dc.subjectimmunostimulation
dc.subjectnonhuman
dc.subjectnucleosome
dc.subjectphagocyte
dc.subjectpriority journal
dc.subjectprognosis
dc.subjectprotein function
dc.subjectReview
dc.subjectsystemic lupus erythematosus
dc.titleThe role of nuclear factors as “Find-Me”/alarmin signals and immunostimulation in defective efferocytosis and related disorders
dc.typeReview


Ficheros en el ítem

Thumbnail
Nombre:
item_2-s2.0-85077660067.pdf
Tamaño:
3.647Kb
Formato:
PDF
Ver/

Este ítem aparece en la(s) siguiente(s) colección(ones)

Mostrar el registro sencillo del ítem