Adults with celiac disease exhibit overexpression of endogenous retroviruses, TRIM28, and SETDB1 despite gluten-free diet
•Celiac disease is immune-mediated and triggered by gluten in predisposed people.•HERVs are viral DNA remnants linked to immune and inflammatory disorders.•The study analyzed HERVs, TRIM28, SETDB1 in 51 celiac adults on gluten-free diet.•CeD patients showed higher HERV and gene expression vs. health...
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| Veröffentlicht in: | Virus research Jg. 359; S. 199613 |
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01.09.2025
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| Abstract | •Celiac disease is immune-mediated and triggered by gluten in predisposed people.•HERVs are viral DNA remnants linked to immune and inflammatory disorders.•The study analyzed HERVs, TRIM28, SETDB1 in 51 celiac adults on gluten-free diet.•CeD patients showed higher HERV and gene expression vs. healthy controls.•Persistent HERV activation may raise long-term autoimmune and cancer risks.
Celiac disease (CeD) is a disorder due to abnormal immune response to gluten protein in individuals with predisposing genotypes. Its origin is not fully understood. Human endogenous retroviruses (HERVs) derive from ancestral infections of germinal cells and represent 8 % of the human DNA. They are mostly inactive, but some can be activated. Their aberrant expressions are associated with inflammatory and immune-mediated diseases. HERV transcription is modulated by TRIM28 and SETDB1, which are also directly implicated in epigenetic processes and modulation of the immune response. We reported HERV overexpressions in CeD children at diagnosis. In the current prospective study, using a PCR real-time Taqman amplification assay, we explored the transcription levels of HERV-H-pol, -HERV-K-pol, and HERV-W-pol, of syncytin 1 (SYN1), SYN2, and HERV-W-env, as well as of TRIM28 and SETDB1 in the whole blood from 51 adults with CeD after years of good compliance with gluten-free diet (GFD) as compared to healthy controls (HC) of similar age.
The transcriptional levels of every HERV and of TRIM28/SETDB1 were significantly higher in CeD patients than in HC (constantly with p < 0.0001). Positive correlations were found between the RNA levels of TRIM28 or SETDB1 and HERVs in CeD patients. The upregulation of HERVs, TRIM28, and SETDB1 and their positive correlations are suggestive clues of their contribution to the pathophysiology of CeD and might justify the persistent risk of developing, despite GFD, autoimmune diseases, neuropsychiatric disturbances, and cancers, all disorders characterized by enhanced HERV expressions and epigenetic alterations. |
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| AbstractList | Celiac disease (CeD) is a disorder due to abnormal immune response to gluten protein in individuals with predisposing genotypes. Its origin is not fully understood. Human endogenous retroviruses (HERVs) derive from ancestral infections of germinal cells and represent 8 % of the human DNA. They are mostly inactive, but some can be activated. Their aberrant expressions are associated with inflammatory and immune-mediated diseases. HERV transcription is modulated by TRIM28 and SETDB1, which are also directly implicated in epigenetic processes and modulation of the immune response. We reported HERV overexpressions in CeD children at diagnosis. In the current prospective study, using a PCR real-time Taqman amplification assay, we explored the transcription levels of HERV-H-pol, -HERV-K-pol, and HERV-W-pol, of syncytin 1 (SYN1), SYN2, and HERV-W-env, as well as of TRIM28 and SETDB1 in the whole blood from 51 adults with CeD after years of good compliance with gluten-free diet (GFD) as compared to healthy controls (HC) of similar age. The transcriptional levels of every HERV and of TRIM28/SETDB1 were significantly higher in CeD patients than in HC (constantly with p < 0.0001). Positive correlations were found between the RNA levels of TRIM28 or SETDB1 and HERVs in CeD patients. The upregulation of HERVs, TRIM28, and SETDB1 and their positive correlations are suggestive clues of their contribution to the pathophysiology of CeD and might justify the persistent risk of developing, despite GFD, autoimmune diseases, neuropsychiatric disturbances, and cancers, all disorders characterized by enhanced HERV expressions and epigenetic alterations.Celiac disease (CeD) is a disorder due to abnormal immune response to gluten protein in individuals with predisposing genotypes. Its origin is not fully understood. Human endogenous retroviruses (HERVs) derive from ancestral infections of germinal cells and represent 8 % of the human DNA. They are mostly inactive, but some can be activated. Their aberrant expressions are associated with inflammatory and immune-mediated diseases. HERV transcription is modulated by TRIM28 and SETDB1, which are also directly implicated in epigenetic processes and modulation of the immune response. We reported HERV overexpressions in CeD children at diagnosis. In the current prospective study, using a PCR real-time Taqman amplification assay, we explored the transcription levels of HERV-H-pol, -HERV-K-pol, and HERV-W-pol, of syncytin 1 (SYN1), SYN2, and HERV-W-env, as well as of TRIM28 and SETDB1 in the whole blood from 51 adults with CeD after years of good compliance with gluten-free diet (GFD) as compared to healthy controls (HC) of similar age. The transcriptional levels of every HERV and of TRIM28/SETDB1 were significantly higher in CeD patients than in HC (constantly with p < 0.0001). Positive correlations were found between the RNA levels of TRIM28 or SETDB1 and HERVs in CeD patients. The upregulation of HERVs, TRIM28, and SETDB1 and their positive correlations are suggestive clues of their contribution to the pathophysiology of CeD and might justify the persistent risk of developing, despite GFD, autoimmune diseases, neuropsychiatric disturbances, and cancers, all disorders characterized by enhanced HERV expressions and epigenetic alterations. •Celiac disease is immune-mediated and triggered by gluten in predisposed people.•HERVs are viral DNA remnants linked to immune and inflammatory disorders.•The study analyzed HERVs, TRIM28, SETDB1 in 51 celiac adults on gluten-free diet.•CeD patients showed higher HERV and gene expression vs. healthy controls.•Persistent HERV activation may raise long-term autoimmune and cancer risks. Celiac disease (CeD) is a disorder due to abnormal immune response to gluten protein in individuals with predisposing genotypes. Its origin is not fully understood. Human endogenous retroviruses (HERVs) derive from ancestral infections of germinal cells and represent 8 % of the human DNA. They are mostly inactive, but some can be activated. Their aberrant expressions are associated with inflammatory and immune-mediated diseases. HERV transcription is modulated by TRIM28 and SETDB1, which are also directly implicated in epigenetic processes and modulation of the immune response. We reported HERV overexpressions in CeD children at diagnosis. In the current prospective study, using a PCR real-time Taqman amplification assay, we explored the transcription levels of HERV-H-pol, -HERV-K-pol, and HERV-W-pol, of syncytin 1 (SYN1), SYN2, and HERV-W-env, as well as of TRIM28 and SETDB1 in the whole blood from 51 adults with CeD after years of good compliance with gluten-free diet (GFD) as compared to healthy controls (HC) of similar age. The transcriptional levels of every HERV and of TRIM28/SETDB1 were significantly higher in CeD patients than in HC (constantly with p < 0.0001). Positive correlations were found between the RNA levels of TRIM28 or SETDB1 and HERVs in CeD patients. The upregulation of HERVs, TRIM28, and SETDB1 and their positive correlations are suggestive clues of their contribution to the pathophysiology of CeD and might justify the persistent risk of developing, despite GFD, autoimmune diseases, neuropsychiatric disturbances, and cancers, all disorders characterized by enhanced HERV expressions and epigenetic alterations. Celiac disease (CeD) is a disorder due to abnormal immune response to gluten protein in individuals with predisposing genotypes. Its origin is not fully understood. Human endogenous retroviruses (HERVs) derive from ancestral infections of germinal cells and represent 8 % of the human DNA. They are mostly inactive, but some can be activated. Their aberrant expressions are associated with inflammatory and immune-mediated diseases. HERV transcription is modulated by TRIM28 and SETDB1, which are also directly implicated in epigenetic processes and modulation of the immune response. We reported HERV overexpressions in CeD children at diagnosis. In the current prospective study, using a PCR real-time Taqman amplification assay, we explored the transcription levels of HERV-H-pol, -HERV-K-pol, and HERV-W-pol, of syncytin 1 (SYN1), SYN2, and HERV-W-env, as well as of TRIM28 and SETDB1 in the whole blood from 51 adults with CeD after years of good compliance with gluten-free diet (GFD) as compared to healthy controls (HC) of similar age. The transcriptional levels of every HERV and of TRIM28/SETDB1 were significantly higher in CeD patients than in HC (constantly with p < 0.0001). Positive correlations were found between the RNA levels of TRIM28 or SETDB1 and HERVs in CeD patients. The upregulation of HERVs, TRIM28, and SETDB1 and their positive correlations are suggestive clues of their contribution to the pathophysiology of CeD and might justify the persistent risk of developing, despite GFD, autoimmune diseases, neuropsychiatric disturbances, and cancers, all disorders characterized by enhanced HERV expressions and epigenetic alterations. •Celiac disease is immune-mediated and triggered by gluten in predisposed people.•HERVs are viral DNA remnants linked to immune and inflammatory disorders.•The study analyzed HERVs, TRIM28, SETDB1 in 51 celiac adults on gluten-free diet.•CeD patients showed higher HERV and gene expression vs. healthy controls.•Persistent HERV activation may raise long-term autoimmune and cancer risks. Celiac disease (CeD) is a disorder due to abnormal immune response to gluten protein in individuals with predisposing genotypes. Its origin is not fully understood. Human endogenous retroviruses (HERVs) derive from ancestral infections of germinal cells and represent 8 % of the human DNA. They are mostly inactive, but some can be activated. Their aberrant expressions are associated with inflammatory and immune-mediated diseases. HERV transcription is modulated by TRIM28 and SETDB1, which are also directly implicated in epigenetic processes and modulation of the immune response. We reported HERV overexpressions in CeD children at diagnosis. In the current prospective study, using a PCR real-time Taqman amplification assay, we explored the transcription levels of HERV-H-pol, -HERV-K-pol, and HERV-W-pol, of syncytin 1 (SYN1), SYN2, and HERV-W-env, as well as of TRIM28 and SETDB1 in the whole blood from 51 adults with CeD after years of good compliance with gluten-free diet (GFD) as compared to healthy controls (HC) of similar age. The transcriptional levels of every HERV and of TRIM28/SETDB1 were significantly higher in CeD patients than in HC (constantly with p < 0.0001). Positive correlations were found between the RNA levels of TRIM28 or SETDB1 and HERVs in CeD patients. The upregulation of HERVs, TRIM28, and SETDB1 and their positive correlations are suggestive clues of their contribution to the pathophysiology of CeD and might justify the persistent risk of developing, despite GFD, autoimmune diseases, neuropsychiatric disturbances, and cancers, all disorders characterized by enhanced HERV expressions and epigenetic alterations. |
| ArticleNumber | 199613 |
| Author | Caviglia, Gian Paolo Galliano, Ilaria Dileo, Eleonora Gambarino, Stefano Armandi, Angelo Tovo, Pier-Angelo Calvi, Cristina Montanari, Paola Bruno, Mauro Pitoni, Demis Ribaldone, Davide Giuseppe Frara, Simone Bergallo, Massimiliano |
| Author_xml | – sequence: 1 givenname: Pier-Angelo surname: Tovo fullname: Tovo, Pier-Angelo email: pierangelo.tovo@unito.it organization: Department of Public Health and Pediatric Sciences, University of Turin, Piazza Polonia 94 10126 Turin, Italy – sequence: 2 givenname: Angelo surname: Armandi fullname: Armandi, Angelo email: angelo.armandi@unito.it organization: Department of Medical Sciences, Division of Gastroenterology and Hepatology, University of Turin, Corso Achille Mario Dogliotti 14 10123, Turin, Italy – sequence: 3 givenname: Mauro surname: Bruno fullname: Bruno, Mauro email: mabru1964@gmail.com organization: Department of Medical Sciences, Division of Gastroenterology and Hepatology, University of Turin, Corso Achille Mario Dogliotti 14 10123, Turin, Italy – sequence: 4 givenname: Gian Paolo surname: Caviglia fullname: Caviglia, Gian Paolo email: gianpaolo.caviglia@unito.it organization: Department of Medical Sciences, Division of Gastroenterology and Hepatology, University of Turin, Corso Achille Mario Dogliotti 14 10123, Turin, Italy – sequence: 5 givenname: Paola surname: Montanari fullname: Montanari, Paola email: paola.montanari@unito.it organization: Pediatric Laboratory, Department of Public Health and Pediatric Sciences, University of Turin, Regina Margherita Children's Hospital, Piazza Polonia 94 10126 Turin, Italy – sequence: 6 givenname: Demis surname: Pitoni fullname: Pitoni, Demis email: pitonidemis@gmail.com organization: Department of Medical Sciences, Division of Gastroenterology and Hepatology, University of Turin, Corso Achille Mario Dogliotti 14 10123, Turin, Italy – sequence: 7 givenname: Cristina surname: Calvi fullname: Calvi, Cristina email: cristina.calvi@unito.it organization: Pediatric Laboratory, Department of Public Health and Pediatric Sciences, University of Turin, Regina Margherita Children's Hospital, Piazza Polonia 94 10126 Turin, Italy – sequence: 8 givenname: Simone surname: Frara fullname: Frara, Simone email: simone.frara@unito.it organization: Department of Medical Sciences, Division of Gastroenterology and Hepatology, University of Turin, Corso Achille Mario Dogliotti 14 10123, Turin, Italy – sequence: 9 givenname: Eleonora surname: Dileo fullname: Dileo, Eleonora email: eleonora.dileo@unito.it organization: Department of Medical Sciences, Division of Gastroenterology and Hepatology, University of Turin, Corso Achille Mario Dogliotti 14 10123, Turin, Italy – sequence: 10 givenname: Stefano surname: Gambarino fullname: Gambarino, Stefano email: stefano.gambarino@unito.it organization: Pediatric Laboratory, Department of Public Health and Pediatric Sciences, University of Turin, Regina Margherita Children's Hospital, Piazza Polonia 94 10126 Turin, Italy – sequence: 11 givenname: Ilaria orcidid: 0000-0002-1273-3178 surname: Galliano fullname: Galliano, Ilaria email: ilaria.galliano@unito.it organization: Pediatric Laboratory, Department of Public Health and Pediatric Sciences, University of Turin, Regina Margherita Children's Hospital, Piazza Polonia 94 10126 Turin, Italy – sequence: 12 givenname: Davide Giuseppe surname: Ribaldone fullname: Ribaldone, Davide Giuseppe email: davidegiuseppe.ribaldone@unito.it organization: Department of Medical Sciences, Division of Gastroenterology and Hepatology, University of Turin, Corso Achille Mario Dogliotti 14 10123, Turin, Italy – sequence: 13 givenname: Massimiliano surname: Bergallo fullname: Bergallo, Massimiliano email: massimiliano.bergallo@unito.it organization: Pediatric Laboratory, Department of Public Health and Pediatric Sciences, University of Turin, Regina Margherita Children's Hospital, Piazza Polonia 94 10126 Turin, Italy |
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| Keywords | Celiac disease Human endogenous retroviruses TRIM28 SETDB1 GFD epigenetics |
| Language | English |
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| Snippet | •Celiac disease is immune-mediated and triggered by gluten in predisposed people.•HERVs are viral DNA remnants linked to immune and inflammatory disorders.•The... Celiac disease (CeD) is a disorder due to abnormal immune response to gluten protein in individuals with predisposing genotypes. Its origin is not fully... |
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| SubjectTerms | Adult Celiac disease Celiac Disease - diet therapy Celiac Disease - genetics Celiac Disease - virology Diet, Gluten-Free Endogenous Retroviruses - genetics epigenetics Female GFD Histone-Lysine N-Methyltransferase - genetics Human endogenous retroviruses Humans Male Middle Aged Prospective Studies SETDB1 TRIM28 Tripartite Motif-Containing Protein 28 - blood Tripartite Motif-Containing Protein 28 - genetics Young Adult |
| Title | Adults with celiac disease exhibit overexpression of endogenous retroviruses, TRIM28, and SETDB1 despite gluten-free diet |
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