Influence of the shared epitope on the elicitation of experimental autoimmune arthritis biomarkers.
Our previous studies have shown that inoculation of the oral cavity of "humanized" B6.DR1/4 mice with the periodontal pathogen Porphyromonas gingivalis results in an increase in the percentage of circulating Th17 cells, loss of bone and an exacerbation of experimental autoimmune arthritis....
| Main Authors: | , , , , , , |
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| Format: | Article |
| Language: | English |
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Public Library of Science (PLoS)
2021-01-01
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| Series: | PLoS ONE |
| Online Access: | https://doi.org/10.1371/journal.pone.0250177 |
| _version_ | 1818083553491025920 |
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| author | Anastasios Karydis Indra Sandal Jiwen Luo Amanda Prislovsky Amanda Gamboa Edward F Rosloniec David D Brand |
| author_facet | Anastasios Karydis Indra Sandal Jiwen Luo Amanda Prislovsky Amanda Gamboa Edward F Rosloniec David D Brand |
| author_sort | Anastasios Karydis |
| collection | DOAJ |
| description | Our previous studies have shown that inoculation of the oral cavity of "humanized" B6.DR1/4 mice with the periodontal pathogen Porphyromonas gingivalis results in an increase in the percentage of circulating Th17 cells, loss of bone and an exacerbation of experimental autoimmune arthritis. The aim of this study was to assess the role played by the human HLA-DRβ molecule containing the shared epitope supplied as a transgene to I-A˚ (murine class II null) C57BL/6 (B6) mice in driving these findings. We compared various immune response parameters as well as alveolar and peri-articular bone loss between humanized B6.DR1 (or B6.DR4) mice and their WT (B6) counterparts. We found that the presence of the shared epitope in the context of inoculation with P. gingivalis enhanced the percentage of Th17 cells generated, dramatically enhanced bone loss and importantly allowed for the generation of CCP2⁺ ACPAs that are not found in C57BL/6 or DBA/1 arthritic mouse serum. Due to the exceedingly complex nature of environmental factors impacting on genetic elements, it has been difficult to unravel mechanisms that drive autoimmune arthritis in susceptible individuals. The findings in this study may provide one small piece of this puzzle that can help us to better understand part of this complexity. |
| first_indexed | 2024-12-10T19:39:50Z |
| format | Article |
| id | doaj.art-cf57c675c5ab45cb9804864c3da466b2 |
| institution | Directory Open Access Journal |
| issn | 1932-6203 |
| language | English |
| last_indexed | 2024-12-10T19:39:50Z |
| publishDate | 2021-01-01 |
| publisher | Public Library of Science (PLoS) |
| record_format | Article |
| series | PLoS ONE |
| spelling | doaj.art-cf57c675c5ab45cb9804864c3da466b22022-12-22T01:36:01ZengPublic Library of Science (PLoS)PLoS ONE1932-62032021-01-01164e025017710.1371/journal.pone.0250177Influence of the shared epitope on the elicitation of experimental autoimmune arthritis biomarkers.Anastasios KarydisIndra SandalJiwen LuoAmanda PrislovskyAmanda GamboaEdward F RosloniecDavid D BrandOur previous studies have shown that inoculation of the oral cavity of "humanized" B6.DR1/4 mice with the periodontal pathogen Porphyromonas gingivalis results in an increase in the percentage of circulating Th17 cells, loss of bone and an exacerbation of experimental autoimmune arthritis. The aim of this study was to assess the role played by the human HLA-DRβ molecule containing the shared epitope supplied as a transgene to I-A˚ (murine class II null) C57BL/6 (B6) mice in driving these findings. We compared various immune response parameters as well as alveolar and peri-articular bone loss between humanized B6.DR1 (or B6.DR4) mice and their WT (B6) counterparts. We found that the presence of the shared epitope in the context of inoculation with P. gingivalis enhanced the percentage of Th17 cells generated, dramatically enhanced bone loss and importantly allowed for the generation of CCP2⁺ ACPAs that are not found in C57BL/6 or DBA/1 arthritic mouse serum. Due to the exceedingly complex nature of environmental factors impacting on genetic elements, it has been difficult to unravel mechanisms that drive autoimmune arthritis in susceptible individuals. The findings in this study may provide one small piece of this puzzle that can help us to better understand part of this complexity.https://doi.org/10.1371/journal.pone.0250177 |
| spellingShingle | Anastasios Karydis Indra Sandal Jiwen Luo Amanda Prislovsky Amanda Gamboa Edward F Rosloniec David D Brand Influence of the shared epitope on the elicitation of experimental autoimmune arthritis biomarkers. PLoS ONE |
| title | Influence of the shared epitope on the elicitation of experimental autoimmune arthritis biomarkers. |
| title_full | Influence of the shared epitope on the elicitation of experimental autoimmune arthritis biomarkers. |
| title_fullStr | Influence of the shared epitope on the elicitation of experimental autoimmune arthritis biomarkers. |
| title_full_unstemmed | Influence of the shared epitope on the elicitation of experimental autoimmune arthritis biomarkers. |
| title_short | Influence of the shared epitope on the elicitation of experimental autoimmune arthritis biomarkers. |
| title_sort | influence of the shared epitope on the elicitation of experimental autoimmune arthritis biomarkers |
| url | https://doi.org/10.1371/journal.pone.0250177 |
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