Expression of HLA-G in human cornea, an immune-privileged tissue

Discorde, Magali Le; Moreau, Philippe; Sabatier, Patrick; Legeais, Jean‐Marc; Carosella, Edgardo D.

doi:10.1016/j.humimm.2003.08.346

Cited by 233 publications

(141 citation statements)

References 27 publications

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“…Surface expression of HLA-E, which is usually weak, can be limited by at least two factors. Surface expression of HLA-E required association with leader peptides derived from HLA-C, HLA-G and -A molecules in a TAP dependent manner (42)(43)(44)(45). HLA-E surface expression is also dependent on availability of 2 microglobulin.…”

Section: Hla-e Molecules Did Not Reach the Surface Of Rabv Infectedmentioning

confidence: 99%

Modulation of HLA-G and HLA-E Expression in Human Neuronal Cells After Rabies Virus or Herpes Virus Simplex Type 1 Infections

et al. 2007

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Abbreviations : RABV (rabies virus), HSV-1 (herpes simplex virus type 1), mAb monoclonal antibody, HCMV ( Human cytomegalovirus) 2 Abstract HLA-G and E are non classical human MHC class I molecules. They may promote tolerance leading to virus and tumour immune escape. We recently described that the herpes simplex virus type 1 (HSV-1), a neurotropic virus inducing chronic infection and neuron latency, and rabies virus (RABV), a neuronotropic virus triggering acute neuron infection -up-regulate HLA-G expression in human neurons (NT2-N). Surface expression was only detected after RABV infection. We investigated here whether RABV and HSV-1 up regulate HLA-E expression in human neuronal precursors (Ntera-2D/1). We found that RABV and -not HSV-1-up regulates HLA-E expression, nevertheless HLA-E could not be detected on the surface of RABV infected Ntera-2D/1. Altogether these data suggest that HLA-G and not HLA-E could contribute to the immune escape of RABV. In contrast, there was no evidence that these molecules are used by latent HSV-1infection. Thus, neurotropic viruses that escape the host immune response totally (RABV) or partially (HSV-1) regulate HLA-G expression on human neuronal cells differentially.3

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Section: Hla-e Molecules Did Not Reach the Surface Of Rabv Infectedmentioning

confidence: 99%

Modulation of HLA-G and HLA-E Expression in Human Neuronal Cells After Rabies Virus or Herpes Virus Simplex Type 1 Infections

et al. 2007

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“…1 HLA-G is normally absent on healthy tissues except trophoblast, 2 thymus 3 and cornea. 4 Interestingly, both HLA-G transcription and protein expression are up-regulated on various tumors cells, as demonstrated in biopsies from patients with melanoma, [5][6][7] breast cancer, 8 renal carcinoma, 9,10 primary cutaneous lymphoma, 11 lung cancer, 12 glioma, 13 epithelial cutaneous malignant lesions 14 and colorectal cancer. 15 .…”

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confidence: 99%

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

et al. 2005

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these points by studying a melanoma cell line derived from a surgically-removed HLA-G-positive melanoma lesion. We show that HLA-G expression in melanoma cells can be regulated at the mRNA splicing level. Indeed, melanoma cells rapidly switched from cell-surface HLA-G1 to intra-cellular HLA-G2 expression. This mechanism restored tumor sensitivity to NK lysis. Moreover, switch from HLA-G1 to HLA-G2 was strong enough to prevent re-expression of immunoprotective HLA-G1 even following treatments with cytokines and DNA demethylating agent. Modulating HLA-G at the mRNA splicing level would be an efficient way of lifting in vivo HLA-G-mediated tumor immune escape. ' 2005 Wiley-Liss, Inc.

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“…HLA-G expression is highly tissue-restricted: besides being expressed in fetal tissues, such as trophoblast cells (Rizzo et al, 2011), HLA-G constitutive expression was found in adult thymic medulla (Mallet et al, 1999), cornea (Le Discorde et al, 2003), pancreatic islets (Cervera et al, 2010) and erythroid and endothelial-cell precursors (Rebmann et al, 2010). However, HLA-G expression can be induced in cancers (Rouas-Freiss et al, 2005), transplantation (Sheshgiri et al, 2010), multiple sclerosis (Wiendl et al, 2005), inflammatory diseases and viral infections (Fainardi et al, 2011).…”

Section: Serum Human Leukocyte Antigen-g and Soluble Interleukin 2 Rementioning

confidence: 99%

Serum Human Leukocyte Antigen-G and Soluble Interleukin 2 Receptor Levels in Acute Lymphoblastic Leukemic Pediatric Patients

Motawi

Zakhary²,

Salman³

et al. 2012

Asian Pacific Journal of Cancer Prevention

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Aims and Background: Human leukocyte antigen-G and interleukin-2 receptor play pivotal roles in the proliferation of lymphocytes, and thus generation of immune responses. Their overexpression has been evidenced in different malignant hematopoietic diseases. This study aimed to validate serum soluble human leukocyte antigen-G (sHLA-G) and serum soluble interleukin-2 receptor (sIL-2R) as an additional tool for the diagnosis and follow up of acute lymphoblastic leukemia (ALL). Subjects and Methods: Both markers were determined by ELISA in the serum of 33 ALL pediatric patients before treatment and after intensification phase of chemotherapy as well as in the serum of 14 healthy donors that were selected as a control group. Results: ALL patients showed abnormal CBC and high serum lactate dehydrogenase, which were improved after chemotherapy. Also, there was a non-significant increase in serum sHLA-G in ALL patients compared with the control group. However, after chemotherapy, sHLA-G was increased significantly compared with before treatment. On the other hand, serum sIL-2R in ALL patients was increased significantly compared with the control group. After chemotherapy, sIL-2R decreased significantly compared with before treatment. Conclusions: From these results it could be suggested that measurement of serum sHLA-G might be helpful in diagnosis of ALL, while sIL-2R might be useful in diagnosis and follow-up of ALL in pediatric patients.Keywords: Soluble human leukocyte antigen-G -soluble interleukin-2 receptor -acute lymphoblastic leukemia

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Expression of HLA-G in human cornea, an immune-privileged tissue

Cited by 233 publications

References 27 publications

Modulation of HLA-G and HLA-E Expression in Human Neuronal Cells After Rabies Virus or Herpes Virus Simplex Type 1 Infections

Modulation of HLA-G and HLA-E Expression in Human Neuronal Cells After Rabies Virus or Herpes Virus Simplex Type 1 Infections

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

Serum Human Leukocyte Antigen-G and Soluble Interleukin 2 Receptor Levels in Acute Lymphoblastic Leukemic Pediatric Patients

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