Blood: Fc-RIIA expression can aggravate nephritis and plateroid intensification of SLE.

Systemic lupus erythematosus (SLE) is an autoimmune inflammatory disease characterized by immune complex (IC) deposition in organs and tissues.
Fc-RIIA, which is expressed in human plateboard, is their unique receptor to IgG antibodies, making them a good response to circulating ICs.
although chronic plateboard active and thrombosis are recognized characteristics of human SLE, the exact mechanism of plateboard active in SLE is not yet clear.
in this study, Melki and others studied the role of Fc-RIIA in SLE and plateboard reaccumification.
in SLE patients, IC levels were associated with plateboard active.
In view of the presence of no Fc-NZ RIIA in mice, the researchers induced FC-RIGIA (FCGR2A) to be induced into SLE's NZB/NZWF1 mouse model, regardless of the plateast response of any SLE model mice to the IC.
, in genetically modified mice, Fc?RIIA is expressed in bone marrow cells, significantly exacerbating lupus nephritis and accelerating death.
Lupus seizures can cause significant changes in plateboard transcription groups, whether in mice that expressed Fc?RIIA or not, but the richness of specific type I interferon-reactive gene changes can be observed in Fc-RIIA-expressed mice.
addition, circulating plateboard granulation and interaction with neutral granulocytes were observed in Fc-RIIA expression mice.
expression of Fc-RIIA in lupus mice can also lead to thrombosis of the lungs and kidneys.
, the model summarizes the characteristics of human SLE and can be used to identify the contribution of different cell linees to SLE performance.
the study further reveals the role of Fc-RIIA in nephritis and plateboard reaccumification in SLE.
.