Human leukocyte antigen G (HLA G) is a major histocompatibility complex (MHC) class I molecule that is primarily expressed in the placenta and is essential for the immune tolerance of the fetus during pregnancy. Unlike many HLA genes, HLA G has relatively few variants and is alternatively spliced into seven different isoforms. Of these isoforms four are membrane-bound while three are predicted to be soluble. Both the membrane-bound and soluble form of HLA G can induce immune tolerance by binding to inhibitory receptors on various immune cells including macrophages and monocytes. HLA G is aberrantly expressed in diseases such as multiple sclerosis, viral infection, and cancer. In cancer HLA G is thought to function as an important mechanism to escape the immune system. Elevated HLA G is found in cancer patient serum and may serve as an important diagnostic tool to distinguish between malignant and benign tumors as well as sensitivity to chemotherapeutic agents.
In a study of a human choriocarcinoma cell line Liu et al. demonstrated the role of HLA G in mediated tumor invasiveness (1). By depleting HLA G with siRNAs and showing protein depletion using the HLA G antibody they were able to show HLA G regulation of STAT3 activation is essential for cell invasion. This study begins to shed light on implantation defects observed with decreased expression of HLA G. In attempt to develop a stem cell based therapy for type I diabetes, Kang et al. cultured neural crest-like cells from humans and differentiated them into insulin producing cells (2). The cells were characterized by flow cytometric analysis using various antibodies to cell surface markers including the HLA G antibody. Transplantation of these cells into a mouse model of diabetes was able to restore insulin levels. Research published by Haider et al. used the HLA G antibody to characterize the role of Notch signaling in the proliferation, differentiation, and motility of human trophoblast cells (3). Using the HLA G antibody as a marker for differentiation the group performed flow cytometry and demonstrated that cultured trophoblast cells undergo spontaneous differentiation and display increased levels of HLA G. Using this system they showed inhibition of Notch signaling enhances the differentiation of trophoblast cells and showed HLA G expression increases through western blots with the HLA G antibody.
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