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HLA‐E polymorphism and soluble HLA‐E plasma levels in chronic hepatitis B patients
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| Zeitschriftentitel: | HLA |
|---|---|
| Personen und Körperschaften: | , , , , , , , , , , , , , , |
| In: | HLA, 87, 2016, 3, S. 153-159 |
| Format: | E-Article |
| Sprache: | Englisch |
| veröffentlicht: |
Wiley
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| Schlagwörter: |
| author_facet |
Zidi, I. Laaribi, A. B. Bortolotti, D. Belhadj, M. Mehri, A. Yahia, H. B. Babay, W. Chaouch, H. Zidi, N. Letaief, A. Yacoub, S. Boukadida, J. Di Luca, D. Hannachi, N. Rizzo, R. Zidi, I. Laaribi, A. B. Bortolotti, D. Belhadj, M. Mehri, A. Yahia, H. B. Babay, W. Chaouch, H. Zidi, N. Letaief, A. Yacoub, S. Boukadida, J. Di Luca, D. Hannachi, N. Rizzo, R. |
|---|---|
| author |
Zidi, I. Laaribi, A. B. Bortolotti, D. Belhadj, M. Mehri, A. Yahia, H. B. Babay, W. Chaouch, H. Zidi, N. Letaief, A. Yacoub, S. Boukadida, J. Di Luca, D. Hannachi, N. Rizzo, R. |
| spellingShingle |
Zidi, I. Laaribi, A. B. Bortolotti, D. Belhadj, M. Mehri, A. Yahia, H. B. Babay, W. Chaouch, H. Zidi, N. Letaief, A. Yacoub, S. Boukadida, J. Di Luca, D. Hannachi, N. Rizzo, R. HLA HLA‐E polymorphism and soluble HLA‐E plasma levels in chronic hepatitis B patients Genetics Immunology Immunology and Allergy |
| author_sort |
zidi, i. |
| spelling |
Zidi, I. Laaribi, A. B. Bortolotti, D. Belhadj, M. Mehri, A. Yahia, H. B. Babay, W. Chaouch, H. Zidi, N. Letaief, A. Yacoub, S. Boukadida, J. Di Luca, D. Hannachi, N. Rizzo, R. 2059-2302 2059-2310 Wiley Genetics Immunology Immunology and Allergy http://dx.doi.org/10.1111/tan.12767 <jats:title>Abstract</jats:title><jats:p>Chronic hepatitis B virus (<jats:styled-content style="fixed-case">HBV</jats:styled-content>) infection occurs in association to a deregulation of immune system. Human leukocyte antigen E (<jats:styled-content style="fixed-case">HLA</jats:styled-content>‐E) is an immune‐tolerant nonclassical <jats:styled-content style="fixed-case">HLA</jats:styled-content> class I molecule that could be involved in <jats:styled-content style="fixed-case">HBV</jats:styled-content> progression. To measure soluble (s) <jats:styled-content style="fixed-case">HLA</jats:styled-content>‐E in patients with chronic <jats:styled-content style="fixed-case">HBV</jats:styled-content> hepatitis (<jats:styled-content style="fixed-case">CHB</jats:styled-content>). We tested the potential association of <jats:italic><jats:styled-content style="fixed-case">HLA</jats:styled-content>‐E*01:01/01:03</jats:italic> A > G gene polymorphism to <jats:styled-content style="fixed-case">CHB</jats:styled-content>. Our cohort consisted of 93 Tunisian <jats:styled-content style="fixed-case">CHB</jats:styled-content> patients (stratified in <jats:styled-content style="fixed-case">CHB</jats:styled-content> with high <jats:styled-content style="fixed-case">HBV DNA</jats:styled-content> levels and <jats:styled-content style="fixed-case">CHB</jats:styled-content> with low <jats:styled-content style="fixed-case">HBV DNA</jats:styled-content> levels) and 245 healthy donors. Plasma <jats:styled-content style="fixed-case">sHLA</jats:styled-content>‐E was determined using enzyme‐linked immunosorbent assay (<jats:styled-content style="fixed-case">ELISA</jats:styled-content>). Genotyping was performed using polymerase chain reaction sequence‐specific primer. No association between <jats:italic><jats:styled-content style="fixed-case">HLA</jats:styled-content>‐E*01:01/01:03</jats:italic> A > G polymorphism and <jats:styled-content style="fixed-case">HBV DNA</jats:styled-content> levels in <jats:styled-content style="fixed-case">CHB</jats:styled-content> patients was found. G/G genotype is less frequent in <jats:styled-content style="fixed-case">CHB</jats:styled-content> patients without significance. <jats:styled-content style="fixed-case">sHLA</jats:styled-content>‐E is significantly enhanced in <jats:styled-content style="fixed-case">CHB</jats:styled-content> patients compared with healthy controls (<jats:italic>P</jats:italic> = 0.0017). Stratification according to <jats:styled-content style="fixed-case">HBV DNA</jats:styled-content> levels showed that <jats:styled-content style="fixed-case">CHB</jats:styled-content> patients with low <jats:styled-content style="fixed-case">HBV DNA</jats:styled-content> levels have higher <jats:styled-content style="fixed-case">sHLA</jats:styled-content>‐E levels compared with <jats:styled-content style="fixed-case">CHB</jats:styled-content> patients with high <jats:styled-content style="fixed-case">HBV DNA</jats:styled-content> levels. <jats:styled-content style="fixed-case">CHB</jats:styled-content> patients with G/G genotype have enhanced <jats:styled-content style="fixed-case">sHLA</jats:styled-content>‐E levels compared with other genotypes (<jats:italic>P</jats:italic> = 0.037). This significant difference is maintained only for <jats:styled-content style="fixed-case">CHB</jats:styled-content> women concerning G/G genotypes (<jats:italic>P</jats:italic> = 0.042). Finally, we reported enhanced <jats:styled-content style="fixed-case">sHLA</jats:styled-content>‐E in <jats:styled-content style="fixed-case">CHB</jats:styled-content> patients with advanced stages of fibrosis (<jats:italic>P</jats:italic> = 0.032). We demonstrate, for the first time, the association of <jats:styled-content style="fixed-case">sHLA</jats:styled-content>‐E to <jats:styled-content style="fixed-case">CHB</jats:styled-content>. Owing to the positive correlation of <jats:italic><jats:styled-content style="fixed-case">HLA</jats:styled-content>‐E*01:01/01:03</jats:italic> A > G polymorphism and the association of <jats:styled-content style="fixed-case">sHLA</jats:styled-content>‐E to advanced fibrosis stages, <jats:styled-content style="fixed-case">HLA</jats:styled-content>‐E could be a powerful predictor for <jats:styled-content style="fixed-case">CHB</jats:styled-content> progression. Further investigations will be required to substantiate <jats:styled-content style="fixed-case">HLA</jats:styled-content>‐E role as a putative clinical biomarker of <jats:styled-content style="fixed-case">CHB</jats:styled-content>.</jats:p> <scp>HLA</scp>‐E polymorphism and soluble <scp>HLA</scp>‐E plasma levels in chronic hepatitis B patients HLA |
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10.1111/tan.12767 |
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Online |
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Biologie Medizin |
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Wiley, 2016 |
| imprint_str_mv |
Wiley, 2016 |
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2059-2302 2059-2310 |
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2059-2302 2059-2310 |
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2016 |
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HLA |
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49 |
| title |
HLA‐E polymorphism and soluble HLA‐E plasma levels in chronic hepatitis B patients |
| title_unstemmed |
HLA‐E polymorphism and soluble HLA‐E plasma levels in chronic hepatitis B patients |
| title_full |
HLA‐E polymorphism and soluble HLA‐E plasma levels in chronic hepatitis B patients |
| title_fullStr |
HLA‐E polymorphism and soluble HLA‐E plasma levels in chronic hepatitis B patients |
| title_full_unstemmed |
HLA‐E polymorphism and soluble HLA‐E plasma levels in chronic hepatitis B patients |
| title_short |
HLA‐E polymorphism and soluble HLA‐E plasma levels in chronic hepatitis B patients |
| title_sort |
<scp>hla</scp>‐e polymorphism and soluble <scp>hla</scp>‐e plasma levels in chronic hepatitis b patients |
| topic |
Genetics Immunology Immunology and Allergy |
| url |
http://dx.doi.org/10.1111/tan.12767 |
| publishDate |
2016 |
| physical |
153-159 |
| description |
<jats:title>Abstract</jats:title><jats:p>Chronic hepatitis B virus (<jats:styled-content style="fixed-case">HBV</jats:styled-content>) infection occurs in association to a deregulation of immune system. Human leukocyte antigen E (<jats:styled-content style="fixed-case">HLA</jats:styled-content>‐E) is an immune‐tolerant nonclassical <jats:styled-content style="fixed-case">HLA</jats:styled-content> class I molecule that could be involved in <jats:styled-content style="fixed-case">HBV</jats:styled-content> progression. To measure soluble (s) <jats:styled-content style="fixed-case">HLA</jats:styled-content>‐E in patients with chronic <jats:styled-content style="fixed-case">HBV</jats:styled-content> hepatitis (<jats:styled-content style="fixed-case">CHB</jats:styled-content>). We tested the potential association of <jats:italic><jats:styled-content style="fixed-case">HLA</jats:styled-content>‐E*01:01/01:03</jats:italic> A > G gene polymorphism to <jats:styled-content style="fixed-case">CHB</jats:styled-content>. Our cohort consisted of 93 Tunisian <jats:styled-content style="fixed-case">CHB</jats:styled-content> patients (stratified in <jats:styled-content style="fixed-case">CHB</jats:styled-content> with high <jats:styled-content style="fixed-case">HBV DNA</jats:styled-content> levels and <jats:styled-content style="fixed-case">CHB</jats:styled-content> with low <jats:styled-content style="fixed-case">HBV DNA</jats:styled-content> levels) and 245 healthy donors. Plasma <jats:styled-content style="fixed-case">sHLA</jats:styled-content>‐E was determined using enzyme‐linked immunosorbent assay (<jats:styled-content style="fixed-case">ELISA</jats:styled-content>). Genotyping was performed using polymerase chain reaction sequence‐specific primer. No association between <jats:italic><jats:styled-content style="fixed-case">HLA</jats:styled-content>‐E*01:01/01:03</jats:italic> A > G polymorphism and <jats:styled-content style="fixed-case">HBV DNA</jats:styled-content> levels in <jats:styled-content style="fixed-case">CHB</jats:styled-content> patients was found. G/G genotype is less frequent in <jats:styled-content style="fixed-case">CHB</jats:styled-content> patients without significance. <jats:styled-content style="fixed-case">sHLA</jats:styled-content>‐E is significantly enhanced in <jats:styled-content style="fixed-case">CHB</jats:styled-content> patients compared with healthy controls (<jats:italic>P</jats:italic> = 0.0017). Stratification according to <jats:styled-content style="fixed-case">HBV DNA</jats:styled-content> levels showed that <jats:styled-content style="fixed-case">CHB</jats:styled-content> patients with low <jats:styled-content style="fixed-case">HBV DNA</jats:styled-content> levels have higher <jats:styled-content style="fixed-case">sHLA</jats:styled-content>‐E levels compared with <jats:styled-content style="fixed-case">CHB</jats:styled-content> patients with high <jats:styled-content style="fixed-case">HBV DNA</jats:styled-content> levels. <jats:styled-content style="fixed-case">CHB</jats:styled-content> patients with G/G genotype have enhanced <jats:styled-content style="fixed-case">sHLA</jats:styled-content>‐E levels compared with other genotypes (<jats:italic>P</jats:italic> = 0.037). This significant difference is maintained only for <jats:styled-content style="fixed-case">CHB</jats:styled-content> women concerning G/G genotypes (<jats:italic>P</jats:italic> = 0.042). Finally, we reported enhanced <jats:styled-content style="fixed-case">sHLA</jats:styled-content>‐E in <jats:styled-content style="fixed-case">CHB</jats:styled-content> patients with advanced stages of fibrosis (<jats:italic>P</jats:italic> = 0.032). We demonstrate, for the first time, the association of <jats:styled-content style="fixed-case">sHLA</jats:styled-content>‐E to <jats:styled-content style="fixed-case">CHB</jats:styled-content>. Owing to the positive correlation of <jats:italic><jats:styled-content style="fixed-case">HLA</jats:styled-content>‐E*01:01/01:03</jats:italic> A > G polymorphism and the association of <jats:styled-content style="fixed-case">sHLA</jats:styled-content>‐E to advanced fibrosis stages, <jats:styled-content style="fixed-case">HLA</jats:styled-content>‐E could be a powerful predictor for <jats:styled-content style="fixed-case">CHB</jats:styled-content> progression. Further investigations will be required to substantiate <jats:styled-content style="fixed-case">HLA</jats:styled-content>‐E role as a putative clinical biomarker of <jats:styled-content style="fixed-case">CHB</jats:styled-content>.</jats:p> |
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| author | Zidi, I., Laaribi, A. B., Bortolotti, D., Belhadj, M., Mehri, A., Yahia, H. B., Babay, W., Chaouch, H., Zidi, N., Letaief, A., Yacoub, S., Boukadida, J., Di Luca, D., Hannachi, N., Rizzo, R. |
| author_facet | Zidi, I., Laaribi, A. B., Bortolotti, D., Belhadj, M., Mehri, A., Yahia, H. B., Babay, W., Chaouch, H., Zidi, N., Letaief, A., Yacoub, S., Boukadida, J., Di Luca, D., Hannachi, N., Rizzo, R., Zidi, I., Laaribi, A. B., Bortolotti, D., Belhadj, M., Mehri, A., Yahia, H. B., Babay, W., Chaouch, H., Zidi, N., Letaief, A., Yacoub, S., Boukadida, J., Di Luca, D., Hannachi, N., Rizzo, R. |
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| description | <jats:title>Abstract</jats:title><jats:p>Chronic hepatitis B virus (<jats:styled-content style="fixed-case">HBV</jats:styled-content>) infection occurs in association to a deregulation of immune system. Human leukocyte antigen E (<jats:styled-content style="fixed-case">HLA</jats:styled-content>‐E) is an immune‐tolerant nonclassical <jats:styled-content style="fixed-case">HLA</jats:styled-content> class I molecule that could be involved in <jats:styled-content style="fixed-case">HBV</jats:styled-content> progression. To measure soluble (s) <jats:styled-content style="fixed-case">HLA</jats:styled-content>‐E in patients with chronic <jats:styled-content style="fixed-case">HBV</jats:styled-content> hepatitis (<jats:styled-content style="fixed-case">CHB</jats:styled-content>). We tested the potential association of <jats:italic><jats:styled-content style="fixed-case">HLA</jats:styled-content>‐E*01:01/01:03</jats:italic> A > G gene polymorphism to <jats:styled-content style="fixed-case">CHB</jats:styled-content>. Our cohort consisted of 93 Tunisian <jats:styled-content style="fixed-case">CHB</jats:styled-content> patients (stratified in <jats:styled-content style="fixed-case">CHB</jats:styled-content> with high <jats:styled-content style="fixed-case">HBV DNA</jats:styled-content> levels and <jats:styled-content style="fixed-case">CHB</jats:styled-content> with low <jats:styled-content style="fixed-case">HBV DNA</jats:styled-content> levels) and 245 healthy donors. Plasma <jats:styled-content style="fixed-case">sHLA</jats:styled-content>‐E was determined using enzyme‐linked immunosorbent assay (<jats:styled-content style="fixed-case">ELISA</jats:styled-content>). Genotyping was performed using polymerase chain reaction sequence‐specific primer. No association between <jats:italic><jats:styled-content style="fixed-case">HLA</jats:styled-content>‐E*01:01/01:03</jats:italic> A > G polymorphism and <jats:styled-content style="fixed-case">HBV DNA</jats:styled-content> levels in <jats:styled-content style="fixed-case">CHB</jats:styled-content> patients was found. G/G genotype is less frequent in <jats:styled-content style="fixed-case">CHB</jats:styled-content> patients without significance. <jats:styled-content style="fixed-case">sHLA</jats:styled-content>‐E is significantly enhanced in <jats:styled-content style="fixed-case">CHB</jats:styled-content> patients compared with healthy controls (<jats:italic>P</jats:italic> = 0.0017). Stratification according to <jats:styled-content style="fixed-case">HBV DNA</jats:styled-content> levels showed that <jats:styled-content style="fixed-case">CHB</jats:styled-content> patients with low <jats:styled-content style="fixed-case">HBV DNA</jats:styled-content> levels have higher <jats:styled-content style="fixed-case">sHLA</jats:styled-content>‐E levels compared with <jats:styled-content style="fixed-case">CHB</jats:styled-content> patients with high <jats:styled-content style="fixed-case">HBV DNA</jats:styled-content> levels. <jats:styled-content style="fixed-case">CHB</jats:styled-content> patients with G/G genotype have enhanced <jats:styled-content style="fixed-case">sHLA</jats:styled-content>‐E levels compared with other genotypes (<jats:italic>P</jats:italic> = 0.037). This significant difference is maintained only for <jats:styled-content style="fixed-case">CHB</jats:styled-content> women concerning G/G genotypes (<jats:italic>P</jats:italic> = 0.042). Finally, we reported enhanced <jats:styled-content style="fixed-case">sHLA</jats:styled-content>‐E in <jats:styled-content style="fixed-case">CHB</jats:styled-content> patients with advanced stages of fibrosis (<jats:italic>P</jats:italic> = 0.032). We demonstrate, for the first time, the association of <jats:styled-content style="fixed-case">sHLA</jats:styled-content>‐E to <jats:styled-content style="fixed-case">CHB</jats:styled-content>. Owing to the positive correlation of <jats:italic><jats:styled-content style="fixed-case">HLA</jats:styled-content>‐E*01:01/01:03</jats:italic> A > G polymorphism and the association of <jats:styled-content style="fixed-case">sHLA</jats:styled-content>‐E to advanced fibrosis stages, <jats:styled-content style="fixed-case">HLA</jats:styled-content>‐E could be a powerful predictor for <jats:styled-content style="fixed-case">CHB</jats:styled-content> progression. Further investigations will be required to substantiate <jats:styled-content style="fixed-case">HLA</jats:styled-content>‐E role as a putative clinical biomarker of <jats:styled-content style="fixed-case">CHB</jats:styled-content>.</jats:p> |
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| spelling | Zidi, I. Laaribi, A. B. Bortolotti, D. Belhadj, M. Mehri, A. Yahia, H. B. Babay, W. Chaouch, H. Zidi, N. Letaief, A. Yacoub, S. Boukadida, J. Di Luca, D. Hannachi, N. Rizzo, R. 2059-2302 2059-2310 Wiley Genetics Immunology Immunology and Allergy http://dx.doi.org/10.1111/tan.12767 <jats:title>Abstract</jats:title><jats:p>Chronic hepatitis B virus (<jats:styled-content style="fixed-case">HBV</jats:styled-content>) infection occurs in association to a deregulation of immune system. Human leukocyte antigen E (<jats:styled-content style="fixed-case">HLA</jats:styled-content>‐E) is an immune‐tolerant nonclassical <jats:styled-content style="fixed-case">HLA</jats:styled-content> class I molecule that could be involved in <jats:styled-content style="fixed-case">HBV</jats:styled-content> progression. To measure soluble (s) <jats:styled-content style="fixed-case">HLA</jats:styled-content>‐E in patients with chronic <jats:styled-content style="fixed-case">HBV</jats:styled-content> hepatitis (<jats:styled-content style="fixed-case">CHB</jats:styled-content>). We tested the potential association of <jats:italic><jats:styled-content style="fixed-case">HLA</jats:styled-content>‐E*01:01/01:03</jats:italic> A > G gene polymorphism to <jats:styled-content style="fixed-case">CHB</jats:styled-content>. Our cohort consisted of 93 Tunisian <jats:styled-content style="fixed-case">CHB</jats:styled-content> patients (stratified in <jats:styled-content style="fixed-case">CHB</jats:styled-content> with high <jats:styled-content style="fixed-case">HBV DNA</jats:styled-content> levels and <jats:styled-content style="fixed-case">CHB</jats:styled-content> with low <jats:styled-content style="fixed-case">HBV DNA</jats:styled-content> levels) and 245 healthy donors. Plasma <jats:styled-content style="fixed-case">sHLA</jats:styled-content>‐E was determined using enzyme‐linked immunosorbent assay (<jats:styled-content style="fixed-case">ELISA</jats:styled-content>). Genotyping was performed using polymerase chain reaction sequence‐specific primer. No association between <jats:italic><jats:styled-content style="fixed-case">HLA</jats:styled-content>‐E*01:01/01:03</jats:italic> A > G polymorphism and <jats:styled-content style="fixed-case">HBV DNA</jats:styled-content> levels in <jats:styled-content style="fixed-case">CHB</jats:styled-content> patients was found. G/G genotype is less frequent in <jats:styled-content style="fixed-case">CHB</jats:styled-content> patients without significance. <jats:styled-content style="fixed-case">sHLA</jats:styled-content>‐E is significantly enhanced in <jats:styled-content style="fixed-case">CHB</jats:styled-content> patients compared with healthy controls (<jats:italic>P</jats:italic> = 0.0017). Stratification according to <jats:styled-content style="fixed-case">HBV DNA</jats:styled-content> levels showed that <jats:styled-content style="fixed-case">CHB</jats:styled-content> patients with low <jats:styled-content style="fixed-case">HBV DNA</jats:styled-content> levels have higher <jats:styled-content style="fixed-case">sHLA</jats:styled-content>‐E levels compared with <jats:styled-content style="fixed-case">CHB</jats:styled-content> patients with high <jats:styled-content style="fixed-case">HBV DNA</jats:styled-content> levels. <jats:styled-content style="fixed-case">CHB</jats:styled-content> patients with G/G genotype have enhanced <jats:styled-content style="fixed-case">sHLA</jats:styled-content>‐E levels compared with other genotypes (<jats:italic>P</jats:italic> = 0.037). This significant difference is maintained only for <jats:styled-content style="fixed-case">CHB</jats:styled-content> women concerning G/G genotypes (<jats:italic>P</jats:italic> = 0.042). Finally, we reported enhanced <jats:styled-content style="fixed-case">sHLA</jats:styled-content>‐E in <jats:styled-content style="fixed-case">CHB</jats:styled-content> patients with advanced stages of fibrosis (<jats:italic>P</jats:italic> = 0.032). We demonstrate, for the first time, the association of <jats:styled-content style="fixed-case">sHLA</jats:styled-content>‐E to <jats:styled-content style="fixed-case">CHB</jats:styled-content>. Owing to the positive correlation of <jats:italic><jats:styled-content style="fixed-case">HLA</jats:styled-content>‐E*01:01/01:03</jats:italic> A > G polymorphism and the association of <jats:styled-content style="fixed-case">sHLA</jats:styled-content>‐E to advanced fibrosis stages, <jats:styled-content style="fixed-case">HLA</jats:styled-content>‐E could be a powerful predictor for <jats:styled-content style="fixed-case">CHB</jats:styled-content> progression. Further investigations will be required to substantiate <jats:styled-content style="fixed-case">HLA</jats:styled-content>‐E role as a putative clinical biomarker of <jats:styled-content style="fixed-case">CHB</jats:styled-content>.</jats:p> <scp>HLA</scp>‐E polymorphism and soluble <scp>HLA</scp>‐E plasma levels in chronic hepatitis B patients HLA |
| spellingShingle | Zidi, I., Laaribi, A. B., Bortolotti, D., Belhadj, M., Mehri, A., Yahia, H. B., Babay, W., Chaouch, H., Zidi, N., Letaief, A., Yacoub, S., Boukadida, J., Di Luca, D., Hannachi, N., Rizzo, R., HLA, HLA‐E polymorphism and soluble HLA‐E plasma levels in chronic hepatitis B patients, Genetics, Immunology, Immunology and Allergy |
| title | HLA‐E polymorphism and soluble HLA‐E plasma levels in chronic hepatitis B patients |
| title_full | HLA‐E polymorphism and soluble HLA‐E plasma levels in chronic hepatitis B patients |
| title_fullStr | HLA‐E polymorphism and soluble HLA‐E plasma levels in chronic hepatitis B patients |
| title_full_unstemmed | HLA‐E polymorphism and soluble HLA‐E plasma levels in chronic hepatitis B patients |
| title_short | HLA‐E polymorphism and soluble HLA‐E plasma levels in chronic hepatitis B patients |
| title_sort | <scp>hla</scp>‐e polymorphism and soluble <scp>hla</scp>‐e plasma levels in chronic hepatitis b patients |
| title_unstemmed | HLA‐E polymorphism and soluble HLA‐E plasma levels in chronic hepatitis B patients |
| topic | Genetics, Immunology, Immunology and Allergy |
| url | http://dx.doi.org/10.1111/tan.12767 |