<?xml version="1.0" encoding="UTF-8"?><xml><records><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Catamo, E</style></author><author><style face="normal" font="default" size="100%">Zupin, L</style></author><author><style face="normal" font="default" size="100%">Freato, N</style></author><author><style face="normal" font="default" size="100%">Polesello, V</style></author><author><style face="normal" font="default" size="100%">Celsi, F</style></author><author><style face="normal" font="default" size="100%">Crocè, S L</style></author><author><style face="normal" font="default" size="100%">Masutti, F</style></author><author><style face="normal" font="default" size="100%">Pozzato, G</style></author><author><style face="normal" font="default" size="100%">Segat, L</style></author><author><style face="normal" font="default" size="100%">Crovella, S</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">HLA-G regulatory polymorphisms are associated with susceptibility to HCV infection.</style></title><secondary-title><style face="normal" font="default" size="100%">HLA</style></secondary-title><alt-title><style face="normal" font="default" size="100%">HLA</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">3' Untranslated Regions</style></keyword><keyword><style  face="normal" font="default" size="100%">5' Untranslated Regions</style></keyword><keyword><style  face="normal" font="default" size="100%">Adult</style></keyword><keyword><style  face="normal" font="default" size="100%">Aged</style></keyword><keyword><style  face="normal" font="default" size="100%">Aged, 80 and over</style></keyword><keyword><style  face="normal" font="default" size="100%">Alleles</style></keyword><keyword><style  face="normal" font="default" size="100%">Case-Control Studies</style></keyword><keyword><style  face="normal" font="default" size="100%">Exons</style></keyword><keyword><style  face="normal" font="default" size="100%">Female</style></keyword><keyword><style  face="normal" font="default" size="100%">Gene Expression</style></keyword><keyword><style  face="normal" font="default" size="100%">Gene Frequency</style></keyword><keyword><style  face="normal" font="default" size="100%">Genetic Association Studies</style></keyword><keyword><style  face="normal" font="default" size="100%">Genetic Predisposition to Disease</style></keyword><keyword><style  face="normal" font="default" size="100%">Haplotypes</style></keyword><keyword><style  face="normal" font="default" size="100%">Hepacivirus</style></keyword><keyword><style  face="normal" font="default" size="100%">Hepatitis C</style></keyword><keyword><style  face="normal" font="default" size="100%">HLA-G Antigens</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Italy</style></keyword><keyword><style  face="normal" font="default" size="100%">Male</style></keyword><keyword><style  face="normal" font="default" size="100%">Middle Aged</style></keyword><keyword><style  face="normal" font="default" size="100%">Polymorphism, Single Nucleotide</style></keyword><keyword><style  face="normal" font="default" size="100%">Risk</style></keyword><keyword><style  face="normal" font="default" size="100%">Th1 Cells</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2017</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2017 03</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">89</style></volume><pages><style face="normal" font="default" size="100%">135-142</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;&lt;b&gt;BACKGROUND: &lt;/b&gt;Hepatitis C virus (HCV) is able to bypass the immune system modulating innate and adaptive immune response and blocking T helper 1 (Th1) cell production. Because the human leukocyte antigen (HLA)-G molecule has immunomodulatory properties inhibiting the function and production of natural killer and cytotoxic lymphocyte T cells, as well as promoting shift from Th1 toward Th2 response, we hypothesized its involvement in susceptibility to HCV infection.&lt;/p&gt;&lt;p&gt;&lt;b&gt;MATERIALS AND METHODS: &lt;/b&gt;Considering that HLA-G mRNA expression has been reported to be under genetic control, an association study was conducted analyzing 800 base pairs upstream the ATG at the 5'upstream regulator region (URR) and 850 base pairs from ATG to exon 3 and the 3'untranslated region (UTR) of HLA-G gene in Italian HCV-positive patients and uninfected controls.&lt;/p&gt;&lt;p&gt;&lt;b&gt;RESULTS: &lt;/b&gt;Four 5'URR polymorphisms (-725C&gt;G&gt;T, -509C&gt;G, -400G&gt;A and -398G&gt;A), 7 polymorphisms at coding region (+15G&gt;A, +36G&gt;A, +243G&gt;A, insC506, 531G&gt;C, delA615 and 685G&gt;A), the +644G&gt;T polymorphism, and 1 haplotype (TTGTTCCIGAC) showed different frequency distributions between HCV patients and uninfected controls.&lt;/p&gt;&lt;p&gt;&lt;b&gt;CONCLUSION: &lt;/b&gt;The results from our study suggest a possible involvement of HLA-G in the risk modulation toward HCV infection.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">3</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/28083985?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Pellegrin, M C</style></author><author><style face="normal" font="default" size="100%">Matarazzo, L</style></author><author><style face="normal" font="default" size="100%">Neri, E</style></author><author><style face="normal" font="default" size="100%">Pennesi, M</style></author><author><style face="normal" font="default" size="100%">Crovella, S</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">HLA-B35, a common genetic trait, in a familial case of Henoch-Schoenlein purpura and Berger's disease.</style></title><secondary-title><style face="normal" font="default" size="100%">Genet Mol Res</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Genet. Mol. Res.</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Adolescent</style></keyword><keyword><style  face="normal" font="default" size="100%">Child</style></keyword><keyword><style  face="normal" font="default" size="100%">Female</style></keyword><keyword><style  face="normal" font="default" size="100%">Genotype</style></keyword><keyword><style  face="normal" font="default" size="100%">Glomerulonephritis, IGA</style></keyword><keyword><style  face="normal" font="default" size="100%">HLA-B35 Antigen</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Male</style></keyword><keyword><style  face="normal" font="default" size="100%">Middle Aged</style></keyword><keyword><style  face="normal" font="default" size="100%">Nephritis</style></keyword><keyword><style  face="normal" font="default" size="100%">Phenotype</style></keyword><keyword><style  face="normal" font="default" size="100%">Purpura, Schoenlein-Henoch</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2014</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2014</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">13</style></volume><pages><style face="normal" font="default" size="100%">2669-73</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Nephritis characterized by IgA mesangial depositions has been described both in Henoch-Schoenlein purpura (HSP) and in Berger's disease (BD), but common genetic traits are still uncertain. We report here the case of two brothers, the first affected by HSP with persistent nephritis and the second by BD, accidentally discovered as silent microhematuria 1 year after HSP onset in the first brother. HLA genotyping demonstrated the presence of HLA-B35 in both patients. Our findings reinforce the need to screen for urinary abnormalities in family members of patients affected by HSP nephritis to identify a silent IgA nephropathy.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">2</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/24782055?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Segat, L</style></author><author><style face="normal" font="default" size="100%">Zupin, L</style></author><author><style face="normal" font="default" size="100%">Kim, H-Y</style></author><author><style face="normal" font="default" size="100%">Catamo, E</style></author><author><style face="normal" font="default" size="100%">Thea, D M</style></author><author><style face="normal" font="default" size="100%">Kankasa, C</style></author><author><style face="normal" font="default" size="100%">Aldrovandi, G M</style></author><author><style face="normal" font="default" size="100%">Kuhn, L</style></author><author><style face="normal" font="default" size="100%">Crovella, S</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">HLA-G 14 bp deletion/insertion polymorphism and mother-to-child transmission of HIV.</style></title><secondary-title><style face="normal" font="default" size="100%">Tissue Antigens</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Tissue Antigens</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Adult</style></keyword><keyword><style  face="normal" font="default" size="100%">Alleles</style></keyword><keyword><style  face="normal" font="default" size="100%">Base Pairing</style></keyword><keyword><style  face="normal" font="default" size="100%">Child</style></keyword><keyword><style  face="normal" font="default" size="100%">Genotype</style></keyword><keyword><style  face="normal" font="default" size="100%">HIV Infections</style></keyword><keyword><style  face="normal" font="default" size="100%">HLA-G Antigens</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">INDEL Mutation</style></keyword><keyword><style  face="normal" font="default" size="100%">Infant</style></keyword><keyword><style  face="normal" font="default" size="100%">Infectious Disease Transmission, Vertical</style></keyword><keyword><style  face="normal" font="default" size="100%">Mothers</style></keyword><keyword><style  face="normal" font="default" size="100%">Polymorphism, Genetic</style></keyword><keyword><style  face="normal" font="default" size="100%">Young Adult</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2014</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2014 Mar</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">83</style></volume><pages><style face="normal" font="default" size="100%">161-7</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;The human leukocyte antigen HLA-G, highly expressed at the maternal-fetal interface, has a pivotal role in mediating immune tolerance. In this study we investigated the influence of HLA-G 14 bp insertion polymorphism in human immunodeficiency virus (HIV)-1 mother-to-child HIV-1 transmission. The 14 bp insertion polymorphism was analyzed among 99 HIV-1 positive mothers and 329 infants born to HIV-positive mothers in Zambia, among whom vertical transmission status and timing had been determined. HLA-G 14 bp insertion polymorphism was detected using a custom TaqMan single nucleotide polymorphisms (SNPs) genotyping assay. Logistic regression was conducted to examine the associations between HLA-G alleles and the risk of HIV transmission. The 14 bp insertion allele was more frequent in HIV exposed-uninfected (EU) infants than in infected infants, and was associated with reduced risk of both in utero (IU) and intrapartum (IP) HIV transmission, after adjusting for maternal cluster of differentiation 4 (CD4) cell count and plasma viral load. Maternal HLA-G 14 bp insertion genotype and HLA-G concordance between mother and child were not associated with the risk of perinatal HIV transmission. The presence of the 14 bp insertion associates with protection toward IU and IP HIV infection in children from Zambia, suggesting that HLA-G could be involved in the vertical transmission of HIV.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">3</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/24571474?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Catamo, E</style></author><author><style face="normal" font="default" size="100%">Addobbati, C</style></author><author><style face="normal" font="default" size="100%">Segat, L</style></author><author><style face="normal" font="default" size="100%">Sotero Fragoso, T</style></author><author><style face="normal" font="default" size="100%">Domingues Barbosa, A</style></author><author><style face="normal" font="default" size="100%">Tavares Dantas, A</style></author><author><style face="normal" font="default" size="100%">de Ataíde Mariz, H</style></author><author><style face="normal" font="default" size="100%">F da Rocha, L</style></author><author><style face="normal" font="default" size="100%">Branco Pinto Duarte, A L</style></author><author><style face="normal" font="default" size="100%">Monasta, L</style></author><author><style face="normal" font="default" size="100%">Sandrin-Garcia, P</style></author><author><style face="normal" font="default" size="100%">Crovella, S</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">HLA-G gene polymorphisms associated with susceptibility to rheumatoid arthritis disease and its severity in Brazilian patients.</style></title><secondary-title><style face="normal" font="default" size="100%">Tissue Antigens</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Tissue Antigens</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">3' Untranslated Regions</style></keyword><keyword><style  face="normal" font="default" size="100%">5' Flanking Region</style></keyword><keyword><style  face="normal" font="default" size="100%">Aged</style></keyword><keyword><style  face="normal" font="default" size="100%">Arthritis, Rheumatoid</style></keyword><keyword><style  face="normal" font="default" size="100%">Brazil</style></keyword><keyword><style  face="normal" font="default" size="100%">Disease Progression</style></keyword><keyword><style  face="normal" font="default" size="100%">DNA Mutational Analysis</style></keyword><keyword><style  face="normal" font="default" size="100%">Female</style></keyword><keyword><style  face="normal" font="default" size="100%">Gene Frequency</style></keyword><keyword><style  face="normal" font="default" size="100%">Genetic Association Studies</style></keyword><keyword><style  face="normal" font="default" size="100%">Genetic Predisposition to Disease</style></keyword><keyword><style  face="normal" font="default" size="100%">Genotype</style></keyword><keyword><style  face="normal" font="default" size="100%">Haplotypes</style></keyword><keyword><style  face="normal" font="default" size="100%">HLA-G Antigens</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Male</style></keyword><keyword><style  face="normal" font="default" size="100%">Middle Aged</style></keyword><keyword><style  face="normal" font="default" size="100%">Polymorphism, Single Nucleotide</style></keyword><keyword><style  face="normal" font="default" size="100%">Risk</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2014</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2014 Sep</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">84</style></volume><pages><style face="normal" font="default" size="100%">308-15</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;We analyzed the possible association between human leukocyte antigen-G (HLA-G) genetic variants, supposed to regulate HLA-G expression, and the susceptibility to develop rheumatoid arthritis (RA) as well as its clinical manifestations. The 5'upstream regulatory region (5'URR) and 3'untranslated region (3'UTR) regions of the HLA-G gene were screened in 127 RA patients and 128 controls: 10 5'URR and 3 3'UTR HLA-G polymorphisms as well as two haplotypes were associated with risk for RA development, while a polymorphism in the 5'URR showed an association with the degree of disease activity. These findings, although the number of cases analyzed is limited and the P-values are modest, indicate a possible association between HLA-G gene polymorphisms and susceptibility to develop RA disease and its severity.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">3</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/24957665?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Segat, L</style></author><author><style face="normal" font="default" size="100%">Crovella, S</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">HLA-G 14bp del/ins genetic variation: association with susceptibility to human immunodeficiency virus-1 vertical transmission but not with human immunodeficiency virus-1 infection through horizontal transmission.</style></title><secondary-title><style face="normal" font="default" size="100%">Tissue Antigens</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Tissue Antigens</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Ethnic Groups</style></keyword><keyword><style  face="normal" font="default" size="100%">Genetic Association Studies</style></keyword><keyword><style  face="normal" font="default" size="100%">Genetic Predisposition to Disease</style></keyword><keyword><style  face="normal" font="default" size="100%">HIV Infections</style></keyword><keyword><style  face="normal" font="default" size="100%">HIV-1</style></keyword><keyword><style  face="normal" font="default" size="100%">HLA-G Antigens</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">INDEL Mutation</style></keyword><keyword><style  face="normal" font="default" size="100%">Infectious Disease Transmission, Vertical</style></keyword><keyword><style  face="normal" font="default" size="100%">Polymorphism, Genetic</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2012</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2012 Jul</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">80</style></volume><pages><style face="normal" font="default" size="100%">12-3</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><issue><style face="normal" font="default" size="100%">1</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/22512775?dopt=Abstract</style></custom1></record></records></xml>