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that CD4+ HLA-G+ Tregs suppressed T-cell proliferation by secreting IL-10 and sHLA-G.43,44 A more recent study by Pankratz et al.45 showed that CD4+ HLA-G+ Tregs are the key player in inflammation and can ameliorate graft-ver- sus-host diseases in vivo. Here, the proportion of CD4+ HLA-G+ cells was significantly decreased in ITP patients,
further establishing the role of HLA-G in reconstructing immune tolerance in ITP patients.
In addition, rhHLA-G exerted their immunosuppres- sive effects by promoting IL-1β, IL-2, G-CSF, and GM- CSF production. A previous study demonstrated that GM-CSF suppresses the immune response by expanding
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Figure 5. rhHLA-G modulation decreased expression of costimulation molecules on dendritic cells and inhibited CD4+ T-cell proliferation by dendritic cells. (A) Representative histograms and (B) analysis of CD86 MFI on dendritic cells from 17 immune thrombocytopenia (ITP) patients and 15 healthy controls. (C) Representative histograms and (D) analysis of CD80 MFI on dendritic cells from 17 ITP patients and 15 healthy controls. *P<0.05; **P<0.01. (E) Representative histograms and (F) analysis of CD4+ T-cell proliferation stimulated by in vitro generated dendritic cells with or without recombinant human leukocyte antigen-G (rhHLA- G) premodulation from 17 ITP patients and 15 healthy controls. *P<0.05; **P<0.01.
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haematologica | 2021; 106(3)