Expression of HLA-G in human mononuclear phagocytes and selective induction by IFN-γ

Switch ofHLA-G alternative splicing in a melanoma cell line causes loss of HLA-G1 expression and sensitivity to NK lysis

“…Similar results were reported for other tumor cell lines. 13,39,[48][49][50][51] Such an observation deserves particular attention in the context of IFN-based immunotherapy or anti-tumor chemotherapy using demethylating drugs such as decitabine in melanoma patients whose immune system may be inhibited by the boosted expression of HLA-G1. 6,7 Interestingly, in our study, the HLA-G switch from HLA-G1 to HLA-G2 was strong enough to prevent reexpression of HLA-G1 mRNA and protein even following treatment with cytokines and DNA demethylating agent.…”

Human immunodeficiency virus 1 downregulates cell surface expression of the non-classical major histocompatibility class I molecule HLA-G1

“…Several studies have reported that Mw can express HLA-G1 (Yang et al, 1996;Onno et al, 2000). To investigate whether HLA-G1 expression was downregulated during HIV-1 infection of primary cultures of human Mw derived from PBMCs, we first analysed HLA-G1 expression in seven different primary cultures of human Mw.…”

“…MHC-I downregulation was shown to be dependent on HIV Nef mainly, affecting endocytosis of classical HLA-A and HLA-B, but not that of HLA-C or of non-classical HLA-E (Cohen et al, 1999;Blagoveshchenskaya et al, 2002). Unlike other MHC-I molecules, HLA-G is characterized by a low polymorphism and a restricted tissue distribution, being found mostly in placental trophoblasts, thymic epithelial cells (Le Bouteiller & Blaschitz, 1999) and macrophages (Mw) (Yang et al, 1996). Moreover, HLA-G is transcribed and translated into multiple membrane-bound and soluble isoforms, as a result of alternative splicing (Ishitani & Geraghty, 1992).…”

Identification of a novel HLA-G+ regulatory population in blood: expansion after allogeneic transplantation and de novo HLA-G expression at graft-versus-host disease sites

“…The existence of HLA-G pos monocytes in steady state blood has been previously reported by different authors. [4][5][6][7] However, other groups could not verify this by using the same antibody (87G). 26 Differences in the purification method used could in part explain the reported discrepancy.…”

“…It has been shown that microenvironmental factors, such as TNFa or interferons which are also identified at GvHD sites, 23 may up-regulate the HLA-G expression. 4,6 However, whether the ectopic HLA-G expression in the skin after transplantation is a consequence of GvHD or is part of an internal regulatory system to control GvHD remains to be defined in prospective, longitudinal studies with a larger study cohort, and with the additional application of sensitive methodologies, such as quantitative PCR determination of HLA-G transcripts. Interestingly, one patient with very severe skin GvHD who died from GvHD-related causes showed com-pletely negative expression of HLA-G, both in epidermis as well as in inflammatory cells of the dermis.…”