HLA-G: a look back, a look forward

Carosella, Edgardo D.; LeMaoult, Joël

doi:10.1007/s00018-010-0577-2

Cited by 9 publications

(8 citation statements)

References 30 publications

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“…This is in contrast to a previous study by Kronsteiner et al [ 24 ] which reported that PTEC alone do not secrete sHLA-G. However, unlike our study, Kronsteiner et al did not stimulate PTEC with IFN-γ, which induces the expression of sHLA-G. Functionally, the role of sHLA-G has been demonstrated to be beneficial in various clinical conditions including pregnancy, transplantation and various inflammatory diseases [ 25 , 26 ]. In kidney models, the presence of HLA-G in renal allograft biopsies [ 27 ] and increased sHLA-G levels in plasma samples from kidney transplant patients [ 28 ] have both correlated with improved kidney graft acceptance.…”

Section: Discussioncontrasting

confidence: 99%

The Mechanisms of Human Renal Epithelial Cell Modulation of Autologous Dendritic Cell Phenotype and Function

et al. 2015

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Proximal tubule epithelial cells (PTEC) of the kidney line the proximal tubule downstream of the glomerulus and play a major role in the re-absorption of small molecular weight proteins that may pass through the glomerular filtration process. In the perturbed disease state PTEC also contribute to the inflammatory disease process via both positive and negative mechanisms via the production of inflammatory cytokines which chemo-attract leukocytes and the subsequent down-modulation of these cells to prevent uncontrolled inflammatory responses. It is well established that dendritic cells are responsible for the initiation and direction of adaptive immune responses. Both resident and infiltrating dendritic cells are localised within the tubulointerstitium of the renal cortex, in close apposition to PTEC, in inflammatory disease states. We previously demonstrated that inflammatory PTEC are able to modulate autologous human dendritic cell phenotype and functional responses. Here we extend these findings to characterise the mechanisms of this PTEC immune-modulation using primary human PTEC and autologous monocyte-derived dendritic cells (MoDC) as the model system. We demonstrate that PTEC express three inhibitory molecules: (i) cell surface PD-L1 that induces MoDC expression of PD-L1; (ii) intracellular IDO that maintains the expression of MoDC CD14, drives the expression of CD80, PD-L1 and IL-10 by MoDC and inhibits T cell stimulatory capacity; and (iii) soluble HLA-G (sHLA-G) that inhibits HLA-DR and induces IL-10 expression by MoDC. Collectively the results demonstrate that primary human PTEC are able to modulate autologous DC phenotype and function via multiple complex pathways. Further dissection of these pathways is essential to target therapeutic strategies in the treatment of inflammatory kidney disorders.

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Section: Discussioncontrasting

confidence: 99%

The Mechanisms of Human Renal Epithelial Cell Modulation of Autologous Dendritic Cell Phenotype and Function

et al. 2015

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“…The mechanisms underlying this lack of protein variability detected for HLA-G are not well understood, mainly because HLA-G is located within the most variable genes of the human genome. This phenomenon is also observed for other non-classical HLA genes such as HLA-E and HLA-F, which present tolerogenic and immune modulatory properties (Rizzo et al, 2008;Donadi et al, 2011;Nilsson et al, 2016;Mendes-Junior et al, 2013;Castelli et al, 2011;Zambra et al, 2016;Hviid et al, 2006;Lima et al, 2016;Castelli et al, 2015;Castelli et al, 2014b;Veiga-Castelli et al, 2016;Dias et al, 2015;Felicio et al, 2014;Veiga-Castelli et al, 2012;Castelli et al, 2007;Hviid et al, 1997;Hviid et al, 1999;Hviid et al, 2001;Hviid et al, 2003;Carosella, 2011;Carosella and LeMaoult, 2011;Arnaiz-Villena et al, 2007a;Arnaiz-Villena et al, 2007b;Alegre et al, 2007;Moscoso et al, 2006;Carvalho dos Santos et al, 2013;Liu et al, 2012). Considering the 500 samples studied here, only six different protein molecules would be encoded by the HLA-G sequences observed: G*01:01 (69.3%), G*01:03 (7.8%), G*01:04 (15.10%), G*01:05N (2.2%), G*01:06 (5.4%) and G*01:11 (0.2%).…”

Section: Discussionmentioning

confidence: 70%

HLA-G variability and haplotypes detected by massively parallel sequencing procedures in the geographicaly distinct population samples of Brazil and Cyprus

Castelli

Gerasimou²,

Paz

et al. 2017

Molecular Immunology

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The HLA-G molecule presents immunomodulatory properties that might inhibit immune responses when interacting with specific Natural Killer and T cell receptors, such as KIR2DL4, ILT2 and ILT4. Thus, HLA-G might influence the outcome of situations in which fine immune system modulation is required, such as autoimmune diseases, transplants, cancer and pregnancy. The majority of the studies regarding the HLA-G gene variability so far was restricted to a specific gene segment (i.e., promoter, coding or 3' untranslated region), and was performed by using Sanger sequencing and probabilistic models to infer haplotypes. Here we propose a massively parallel sequencing (NGS) with a bioinformatics strategy to evaluate the entire HLA-G regulatory and coding segments, with haplotypes inferred relying more on the straightforward haplotyping capabilities of NGS, and less on probabilistic models. Then, HLA-G variability was surveyed in two admixed population samples of distinct geographical regions and demographic backgrounds, Cyprus and Brazil. Most haplotypes (promoters, coding, 3'UTR and extended ones) were detected both in Brazil and Cyprus and were identical to the ones already described by probabilistic models, indicating that these haplotypes are quite old and may be present worldwide.

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“…The HLA expression at feto‐maternal interface can be associated with a successful pregnancy (Ellis, Palmer, & McMichael, ; Kovats et al, ). HLA‐G (OMIM: 142871) is normally expressed in several locations such as fetal trophoblasts, pancreatic islets, and endothelial precursors (Carosella & LeMaoult, ). HLA‐G protects fetal trophoblast cells toward the maternal uterine NK cells during pregnancy (Abediankenari, Farzad, Rahmani, & Hashemi‐Soteh, ).…”

Section: Human Leukocyte Antigensmentioning

confidence: 99%

Genetics of recurrent pregnancy loss among Iranian population

Moghbeli

2019

Molec Gen & Gen Med

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Background Recurrent pregnancy loss (RPL) is one of the most common reproductive disorders which is defined as the occurrence of recurrent miscarriage before 24 weeks of gestation and is observed among 1%–5% of women. Methods Various factors are associated with RPL such as immunological disorders, maternal age, obesity, alcohol, chromosomal abnormality, endocrine disorders, and uterine abnormalities. About half of the RPL cases are related with chromosomal abnormalities. Therefore, RPL genetic tests are mainly limited to karyotyping. However, there is a significant proportion of RPL cases without any chromosomal abnormalities that can be related to the single‐gene aberrations. Therefore, it is required to prepare a diagnostic panel of genetic markers besides karyotyping. Results In the present review, we have summarized all the significant reported genes until now which are associated with RPL among Iranian women. We categorized all the reported genes based on their cellular and molecular functions in order to determine the molecular bases of RPL in this population. Conclusion This review paves the way of introducing a population‐based diagnostic panel of genetic markers for the first time among Iranian RPL cases. Moreover, this review clarifies the genetic and molecular bases of RPL in this population.

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HLA-G: a look back, a look forward

Cited by 9 publications

References 30 publications

The Mechanisms of Human Renal Epithelial Cell Modulation of Autologous Dendritic Cell Phenotype and Function

The Mechanisms of Human Renal Epithelial Cell Modulation of Autologous Dendritic Cell Phenotype and Function

HLA-G variability and haplotypes detected by massively parallel sequencing procedures in the geographicaly distinct population samples of Brazil and Cyprus

Genetics of recurrent pregnancy loss among Iranian population

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