Blood: Fc-RIIA expression aggravates lupus nephritis and promotes plate plateboard resuscing

Systemic lupus erythematosus (SLE) is an autoimmune inflammatory disease characterized by the deposition of immune complexes (ICs) in organs and tissues.
Fc-RIIA is a specific subject of immunoglobulin G antibodies, expressed in human plateplates, and Fc-RIIA's expression enables plates to react ideally to circulating ICs.
although chronic plateplate activity and thrombosis are recognized as human SLE characteristics, the exact mechanism of plate plateboard biosis in SLE is still unclear.
study, Imene and others evaluated the role of Fc-RIIA in SLE and plate plateboard resuscing.
SLE mouse model of FC-RIIA, an expression, IC levels were associated with plateplate activity in SLE patients.
Because the Fc-RIIA gene was missing in mice and in any existing mouse model of lupus, mouse plateplates did not respond to IC, the researchers imported the Fc-RIIA (FCGR2A) gene into the NZB/NZWF1 lupus mouse model.
in a newly established mouse model based on plate activation of IC-Fc-RIIA mediated human SLE, bone marrow cell expression Fc-RIIA significantly aggravated lupus nephritis and accelerated mouse death.
lupus attacks can cause significant changes in plateplate transcription groups, whether in mice that express or do not express Fc'riia, but specifically observed rich changes in type I interferon reaction genes in Fc's RIIA mice.
, circulating platelet departitation particles were observed in lupus mice expressing Fc-RIIA and interacted with neutral granulocytes.
expression of Fc-RIIA in lupus mice can also lead to thrombosis in the lungs and kidneys.
, the model summarizes the characteristics of human SLE and can be used to identify the role of different cell line in SLE performance.
the study further revealed the role of Fc-RIIA in nephritis and SLE plate plateboard resurgeonization.
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